COMBINED INTERNAL MEDICINE NOTES

CAT-1

Prepared by STUDENTS GOVERNMENT OFFICE

MINISTER OF EDUCATION: Basley M. Alex
DEPUTY MINISTER OF EDUCATION: Happyness N. Jackson
[email protected]
INTERNAL MEDICINE
Topic List
(CAT 1)
1.Poliomyelitis and STROKE
2.Epilepsy
3.Diabetes Mellitus
4.Bronchial Asthma
5.Chronic Obstructive Pulmonary Disease(chronic bronchitis and Emphysema)
6.Pulmonary Embolism
7.Bronchiectasis
8.Hypertension
9.HeartFailure
POLIOMYELITIS

DR.MUTTA
Definition
• Poliomyelitis (polio): An acute viral disease, highly infectious, caused
by a polio virus.
• It invades the nervous system, and can present with a wide range of
clinical presentation, from asymptomatic infection to paralytic disease.
• It can strike at any age, but affects mainly children under three (over
50% of all cases).
Poliomyelitis was until recently endemic worldwide infecting infants
and producing paralytic poliomyelitis.
• Like measles, polio infection gives a lifelong immunity.
• Reservoir of infection is a person with asymptomatic infection, mostly
children.
• Poliovirus can spread widely before cases of paralysis are seen.
Polio Virus
• Poliovirus belongs to the genus Enterovirus.
• This group of RNA viruses prefers to inhabit the gastrointestinal tract.
• Polio virus infects and causes disease in humans alone.
• It is composed of a single RNA genome enclosed in a protein shell called a capsid which
protect the virus’s genetic material, and enable poliovirus to infect certain types of cells.
• Three serotypes of poliovirus have been identified-poliovirus.
o Type 1 (PV1)
o Type 2 (PV2)
o Type 3 (PV3)
• All three are extremely virulent and produce the same disease symptoms.
• PV1 is the most commonly encountered form, and the one most closely associated with
paralysis.
Transmission
• The disease is transmitted primarily via the faecal-oral route, by
ingesting contaminated food or water.
• The virus enters through the mouth and nose, multiplies in the throat
and intestinal tract, and then is absorbed and spread through the blood
and lymph system.
• incubation period , is usually 6 to 20 days, with a maximum rane of 3
to 35 days
Polio is most infectious between 7-10 days before and 7-10 days after the
appearance of
symptoms, but transmission is possible as long as the virus remains in the saliva
or
faeces.
• Poliovirus enters the body through the mouth, infecting the first cells it comes
in contact
with i.e. the pharynx (throat) and intestinal mucosa.
• It gains entry by binding to an immunoglobulin-like receptor, known as the
poliovirus
receptor, on the cell surface.
• The virus then hijacks the host cell's own machinery, and begins to replicate.
• Poliovirus divides within gastrointestinal cells for about a week, from where
it spreads to
the tonsils (specifically the follicular dendritic cells residing within the tonsilar
germinalcenters),
the intestinal lymph nodes including the cells of Peyer's patches, and the deep
cervical and mesenteric lymph nodes, where it multiplies abundantly.
• This sustained replication causes a major viremia, and leads to the
development of minor
influenza-like symptoms.
Once established in the intestines, poliovirus can enter the blood stream and
invade the
central nervous system - spreading along nerve fibres.
• As it multiplies, the virus destroys nerve cells (motor neurons) which activate
muscles.
• These nerve cells cannot be regenerated and the affected muscles no longer
function.
• The muscles of the legs are affected more often than the arm muscles.
• The limb becomes floppy and lifeless - a condition known as acute flaccid
paralysis
(AFP).
• More extensive paralysis, involving the trunk and muscles of the thorax and abdomen,
can result in quadriplegia.
• In the most severe cases (bulbar polio), poliovirus attacks the motor neurons of the
brain
stem - reducing breathing capacity and causing difficulty in swallowing and speaking.
• The anterior horn cells of the spinal cord are susceptible to infection with poliovirus
and
are damaged or completely destroyed.
• The risk of paralysis increases with age in non-immunised persons.
• People who are infected after the age of 20 years have much greater risk of getting
paralysis.
Clinical Features of Poliomyelitis
• Two basic patterns of polio infection are described:
o A minor illness which does not involve the central nervous system
(CNS), sometimes
called abortive poliomyelitis.
o A major illness involving the CNS, which may be paralytic or non-
paralytic.
• From these forms the disease is classified into the following forms:
o Asymptomatic 90–95%
o Minor illness 4–8%
o Major illness which can be divided into:
􀂃 Non-paralytic aseptic meningitis 1–2%
􀂃 Paralytic poliomyelitis 0.1–0.5%
􀂃 Spinal polio 79% of paralytic cases
􀂃 Bulbospinal polio 19% of paralytic cases
􀂃 Bulbar polio 2% of paralytic cases
In most people with a normal immune system, a poliovirus infection is
asymptomatic.
• Minor illness may present with the following features:
o General discomfort or uneasiness (malaise), upper respiratory tract infection (sore
throat influenza-like illnesses and fever), gastrointestinal disturbances lasting 1 -2
days (nausea, vomiting, abdominal pain, constipation or, rarely, diarrhoea) and
headache.
• The minor illness cannot be differentiated from other mild viral infections and is
only
recognizable during epidemic of polio.
• After the mild illness, the disease sometimes progresses into the major illness
with a
recurrence of fever.
• In the major illness (non-paralytic poliomyelitis) may or may not be preceded
by the
minor illness, it present with the following features;
o Back pain, diarrhoea and vomiting, excessive tiredness, headache, irritability,
leg pain
(calf muscles), moderate fever, muscle stiffness, muscle tenderness and spasm in
any
area of the body like the neck.
Divisions of the Major Illness
• Pre-paralytic stage: the temperature rises rapidly to 39 - 40oC with headache and signs of
meningeal irritation.
o The general symptoms return; Malaise, vomiting anorexia and diarrhoea and after 1-2
days, the symptoms disappear.
o The patient may recover or may go on to the next stage known as the paralytic stage.
• Paralytic stage: Paralysis can appear at any site of the body and is asymmetrical.
o The lower limbs are more often affected than the upper.
o Spread of paralysis is usually completed in twenty four hours.
o The paralysed muscles are painful.
o Physical activities at the time of the temporary improvement may aggravate the
degree of subsequent paralysis.
• Post-Paralytic stage: This is the stage of residual disability.
o Paralysis or weakness of muscles will lead to deformity and
contractures.
o A severely affected limb will show effects of abnormalities in blood
circulation such
as coldness and cyanosis.
o There may be retardation of bone growth resulting in shortening of
the affected limb.
Paralytic Poliomyelitis
• Paralytic poliomyelitis is classified as spinal, bulbar, or bulbospinal.
Spinal Polio
• Is the most common form of paralytic poliomyelitis; it results from
viral invasion of the
motor neurons of the anterior horn cells, or the ventral (front) gray
matter section in the
spinal column, which are responsible for movement of the muscles, of the trunk, limbs
and intercostals.
• Virus invasion causes inflammation of the nerve cells, leading to damage or destruction
of motor neuron ganglia.
• When spinal neurons die, leads to weakness of those muscles formerly innervated by the
now dead neurons.
• With the destruction of nerve cells, the muscles no longer receive signals from the brain
or spinal cord; without nerve stimulation, the muscles atrophy, becoming weak, floppy
and poorly controlled, and finally completely paralyzed.
Bulbar Polio
• Bulbar polio occurs when poliovirus invades and destroys nerves within the
bulbar region
of the brain stem.
• The bulbar region is a white matter pathway that connects the cerebral cortex to
the brain
stem.
• The destruction of these nerves weakens the muscles supplied by the cranial
nerves,
producing symptoms of encephalitis, and causes difficulty breathing, speaking and
swallowing.
• Critical nerves affected are the glossopharyngeal nerve, which partially controls
swallowing and functions in the throat, tongue movement and taste; the vagus nerve,
which sends signals to the heart, intestines, and lungs; and the accessory nerve,
which controls upper neck movement.
• Other signs and symptoms include facial weakness, caused by destruction of the
trigeminal nerve and facial nerve, which innervate the cheeks, tear ducts, gums, and
muscles of the face, among other structures; double vision; difficulty in chewing; and
abnormal respiratory rate, depth, and rhythm, which may lead to respiratory arrest.
Possible Complications
• Complications from prolonged immobility include aspiration pneumonia, Corpulmonale,
Pulmonary oedema, myocarditis, high blood pressure, kidney stones, urinary tract
infections and paralytic ileus (loss of intestinal function)
• Muscle paresis and paralysis can sometimes result in skeletal deformities, tightening of
the joints and movement disability.
• A typical manifestation of this problem is equinus foot (similar to club foot).
• Osteoporosis and increased likelihood of bone fractures may occur.
• Extended use of braces or wheelchairs may cause compression neuropathy, as well as a
loss of proper function of the veins in the legs, due to pooling of blood in paralyzed lower
limbs.
• Step 4: Management of Poliomyelitis (15 minutes)
• Diagnosis
• • Paralytic poliomyelitis may be clinically suspected in individuals experiencing acute
• onset of flaccid paralysis in one or more limbs with decreased or absent tendon reflexes in
• the affected limbs.
• • When suspecting a case of polio or any case of acute flaccid paralysis inform DMO
• • Collect and send specimen to district hospital where they will send it central laboratory
• for:
• o Diagnosis of polio.
• o This is made by isolation of the polio virus from stool, throat specimens, and urine.
• o Detection of virus in the CSF is diagnostic of paralytic polio, but rarely occurs.
• o Stool cultures are most likely to yield the organism.
• o If poliovirus is isolated from a patient experiencing acute flaccid paralysis, can be
• further tested through PCR amplification.
• o Antibodies to poliovirus can be diagnostic, and are generally detected in the blood of
• infected patients early in the course of infection
Treatment
• No specific drug available for the poliomyelitis viral infection.
• The focus of modern treatment is to provide relief of symptoms, speeding recovery and
preventing complications.
• Absolute bed rest is necessary in pre-paralytic stage until it is certain that paralysis will
not develop.
• All injections should be avoided for fear of precipitating paralysis
• In the paralytic stage, mobility by passive movements of the affected limb must be
maintained to prevent contractures
• In the post-paralytic stage of the disease, active physiotherapy should be started.
• Refer paralytic patients for physiotherapy as soon as the acute stage is over.
• Disease is contagious-universal precautions and good hand washing are important to
prevent the spread of the disease
Prevention and control
Poliomyelitis is a notifiable disease.
• Inform DConfirm cases by sending fresh stool samples immediately to the nearest reference
laboratory.
• It is essential to immunize all contacts and ensure high coverage in the immunity.
• This will lead to the eradication of a disease.
• Eradication is defined as zero cases of paralytic poliomyelitis due to wild poliovirus
infection and the absence of environmental circulation of wild poliovirus: three years'
absence of wild poliovirus qualifies a region as having eradicated polio. WHO
recommends four strategies for achieving this goal:
o Increasing and sustaining coverage with oral polio vaccine
o Conducting national immunization days
o Developing surveillance for acute flaccid paralysis, including laboratory confirmation
o ‘Mopping up’ vaccination campaigns
• The first three strategies are implemented in our country
• The mass polio vaccination campaign now going on in our country involves giving two
doses of oral polio vaccine to all children in the target age group (generally below 5 years
of age) irrespective of prior vaccination history, with an interval of four to six weeks
between the doses.
• There is well established program of immunization for all under five.MO when new paralytic case is suspected.
STROK
E (CVA)

Dr.MUTTA
 DEFINITION

•Stroke denotes the sudden development

of focal neurological deficits related to
impaired cerebral blood flow to the brain.
• This results from damage to an artery
supplying blood to the brain.
A syndrome of focal or global neurologic deficit
that develops suddenly and lasts more than 24
hours in a person with no history of recent head
injury. If < 24 hours, it is called a transient ischemic
attack (TIA).
Blood Supply of the Brain
• Arterial supply of the
brain is derived from 2
pairs of vessels-----
Internal Carotid
Arteries and the
Vertebral Arteries.
Arterial Supply of the CNS
• MCA-lateral surfaces of the frontal,occipital, temporal and parietal
lobes, and insula.
Vertebral-Basilar System
• Supplies the brainstem and parts of the cerebrum and spinal cord.
• Gets blood supply from the subclavian artery.

Basilar
Artery

Vertebral
Aretries
Effects of Blood Supply damage
• Normal blood flow is 55ml/100g of CNS.

• Reduction to about 20ml/100g causes neurons to stop generating

electrical signals.

• Reduction to about 10ml/100g results in necrosis in brain tissue

(infarct) and eventually a stroke.
Epidemiology of stroke
• Is the leading cause of neurological disease and death worldwide

• Approximately 80% of strokes are ischemic

• 20% are hemorrhagic

• KCMC: 67% ischaemic Vs 33% hemorrhagic

• In some literature hemorrhage has large percent

Risk factors
• Controllable; -
Hypertension
Tobacco use
 Diabetes Mellitus.
Hyperlipidaemia- cholesterol level> 5.2mmol/l.
Heart diseases, which are; Myocardial infarction, cardiac arrthymias,
infective endocarditis, cardiomyopathies.
Sickle cell disease.
Obesity
 Risk factors

• Uncontrollable; -
• Age >60 years
• Family history of stroke
• Previous stroke
• Previous transient ischaemic Attack [TIA]
• Male gender
• Geographical location.
nb:Main risk factors for stroke in Africa are hypertension (#1),
DM, hypercholesterolemia, smoking, atrial fibrillation,
rheumatic heart disease, sickle cell anemia, and HIV.
 Aetiology
• Cerebral infarction (CI) - 85%
• Intracranial hemorrhage
hemorrhage in the brain parenchyma this is a Primary intracerebral haemorrhage
(PICH) - 10%
 hemorrhage in the subarachnoid space this is Subarachnoid haemorrhage (SAH) -
5%
• Cerebral venous thrombosis - < 1%
Hemorrhagic Stroke Epidemiology:
Less common (15%) but more severe. Usually occurs in elderly patients or middle
aged patients with severe hypertension.
Patients often present with coma, headache and/or vomiting. Otherwise, symptoms
are similar to ischemic stroke (see above). Almost 50% mortality in the first week.
More of these patients will be referred to hospitals like BMC due to the severity of
their stroke.
Types of Stroke
• There are two types:

1. Ischemic - occlusion of vessels by thrombus or

embolus.

2. Hemorrhagic - rupture of vessels causing either

intracerebral (ICH) or subarachnoid bleeding (SAH)
ISCHEMIC CVA
• Results from low cerebral blood flow usually
because of occlusion of an artery vessel supplying
blood to the brain

• Localized to the area of occlusion

• If contralateral established (via circle of willis),

damage less permanent
Ischemic Stroke
Epidemiology/Natural History:
More common and accounts for 85% of all strokes. Usually
occurs in elderly patients except in cases of sickle cell anemia or
rheumatic heart disease.
Mortality rate is low in the first week (10-20%) but many
patients will die of complications in the first 1-2 months
including: aspiration pneumonia, septic decubitus ulcers and
DVT.
Etiologies  Thrombotic – usually related to atherosclerosis 
Embolic – as with atrial fibrillation, rheumatic heart disease or
endocarditis
ASSESSMMENT AND DIAGNOSIS OF
ISCHEMIC STROKE
• Sudden onset or gradual onset of focal neurologic signs
• Common pattern associated with a stroke are hemiparesis, aphasia,
sensory loss, one sided visual field defect, dysarthria, difficult in
reading and writing or calculating, disorientation, seizures
• Brain stem/cerebellum/posterior hemisphere: Motor or sensory loss
in all four limbs, limb or gait ataxia, dysarthria, nystagmus, amnesia,
bilateral visual field defects, altered level of consciousness
Symptoms and Signs: The most common symptoms/signs of stroke
are
hemiparalysis, aphasia and coma. Signs and symptoms of ischemic
strokes are variable depending on the artery and part of the brain that
is affected
• . For example:
 Anterior Cerebral Artery - Hemiplegia (leg>arm); Confusion, urinary
incontinence, primitive reflexes
 *Middle Cerebral Artery* (Most Common) - Hemiplegia (face/arm>leg);
hemianesthesia; aphasia (if dominant hemisphere)
 Posterior Cerebral Artery - Thalamic syndromes with contralateral
hemisensory disturbance
 Lacunar (involving internal capsule)- Pure hemiplegia
DIAGNOSIS
• Non contrast CT brain scan, ECG, CXR, ECHO, FBC, Electrolyte, Renal and
Hepatic function, EEG is performed if seizure present
• Lumbar puncture and fundoscopy if SAH is suspected
Physical Exam:
Perform a close cardiovascular exam for rhythm, murmurs, carotid and subclavian bruits;
look for signs of peripheral emboli such as Janeway lesions or splinter hemorrhage. Do a
complete and thorough neurological exam.
Diagnostic Studies
 Most important: urgent noncontrast head CT if available (will help differentiate between
ischemic vs hemorrhagic stroke)
 blood work should include at least a HIV Test, CBC, creatinine, lipids, glucose and
electrolytes (to r/o electrolyte imbalance or hypoglycemia as cause of symptoms); PT/PTT
if you are considering a hemorrhagic stroke as you may want to reverse coagulopathies
 Consider EKG
 Consider carotid Doppler if available
 Consider TTE if available (to look for vegetations or thrombus)
Treatment  Consider thrombolysis (if available) if onset of symptoms is within 3 hours,
there is a large deficit, and there is no evidence of hemorrhage or other contraindications
to lysis  We usually do not perform lysis in our setting.
 HEMORRHAGIC CVA
• Occurs suddenly
• Results from arteriosclerosis or severe hypertension
• May occur during activity due to increase in rate heart pumps blood through
vessels
• Caused by a rupture in a small cerebral artery
• Ruptured artery →inflammation of brain tissue →↑ICP →both cerebral
hemisphere damage →death
• Clinical Manifestations
•  ICH: sudden impairment in level of consciousness, vomiting, +/- headache, may
see progressive focal neurologic deficit depending on site of bleeding
 SAH: severe headache, nausea and vomiting, often described as ‘thunderclap’,
can see nuchal rigidity (blood is a meningeal irritant), impairment in level of
consciousness
 subtypes of brain hemorrhage
• ICH (intracerebral haemorrhage): bleeding directly into the brain
parenchyma (arterioles or small arteries).
• Blood accumulation →cerebral edema + ↑ICP
• Commonest causes of ICH are HTN, trauma, bleeding diatheses,
anticoagulant, thrombolytic therapy, vascular malformations (aneurisms,
AVM)
• Physical Exam/Diagnostic Studies
 similar to exam/workup for ischemic stroke
 consider an LP to check for xanthochromia if you are suspicious for SAH
Etiologies
 Intracerebral (ICH): usually associated with HTN, sometimes coagulopathy
 Subarachnoid Hemorrhage (SAH): RARE; ruptured aneurysm, trauma
ASSESSMENT AND Dx OF ICH
• Critical ill patient who often unconscious

• Need History from relatives

• Sudden onset of focal deficit often a/c (ASSOCIATED WITH) severe

headache, nausea, vomiting and rapid neurologic deterioration

• 50% of pts sustain early LOC (key differential from ischemic

stroke)

• Vital signs-high BP (220/100 to 250/150mmhg) signs of increased

ICP

Dx :CT brain scan

FIRST AID MANAGEMENT OF CVA
Faced with unconscious patient suspected to have stroke,
• Airway – Ensure a free airway and adequate respiratory function by
• Lying the patient flat and turned semi prone with a slight head-down
posture to allow any secretions to run out of the mouth.
• Suction to remove any secretions
• Removing all loose dentures
• Insert airway
• Put nasogastric tube (NGT)
Cont….
• Conscious patients should be laid flat in a comfortable position.
• Vital signs
• Level of consciousness
• Intravenous fluids – May not be necessary unless in case of severe hypotension and for
intravenous drugs administration.
• Do the basic investigations available.
 Blood slide for malaria parasites
 Random Blood sugar
 Urinalysis
 Chest X-ray
 Fundoscopy
 Lumbar puncture
 CT -Intracerebral hemorrhage in the parietal
lobe
CT - Middle cerebral artery infarction

hypodense area consistent with acute ischaemic stroke

ISCHAEMIC STROKE MGT

• ABCs as before
• Thrombolitics if presented in few hrs eg. Urokinase,
streptokinase etc
• Anticoagulation therapy ( heparin, warfarin)
• Antiplatelets therapy (Junior ASA, Clopidogrel)
• Identify and treat treatable causes
• Early rehabilitation (physiotherapy, ocupational
therapy, speech therapy etc)
• Nursing care
• Nutrition
start ASA 150mg daily x 30 days (only if can r/o hemorrhagic stroke by CT)
BP should not be lowered in the first 48 hours unless it is very severe (SBP
>200) After 48 hours, lower blood pressure slowly
start statin (simvastatin 20mg)
 start ranitidine or a PPI to prevent stress ulcers
start subcutaneous heparin to prevent a DVT (if can rule out hemorrhagic
bleed)
change position every 4-6 hours to prevent decubitus ulcers
keep the head of the bed elevated to prevent aspiration
watch for signs of cerebral edema/elevated ICP (usually peaks at 3-4 days
post stroke); if evidence of elevated ICP (like declining GCS or papilledema)
start mannitol
after 48 hours, start Physical Therapy! Physical therapy is very important in
stroke management. It should be started early and continued for at least 2-3
months
HEMORRHAGIC CVA MGT
• ABCs
• Identify treatable causes (eg BP, sugar)
• Treat ↑ICP by steroids and/or mannitol
• May need surgical decompression
• Control of epilepsy
• Nursing care
• Feeding
• Rehabilitation
Treatment
 reverse any coagulopathies
 BP control with goal of SBP 140-160 to prevent further bleeding  ranitidine
to prevent stress ulcers
 consider nimodipine (a CCB) and phenytoin if suspect SAH as they decreases
the risk of vasospasm and seizure in these patients
 change positions, raise head of bed and start physical therapy as in ischemic
stroke
REHABILITATION
• Early involvement in physiotherapy
• Occupational and speech and language therapy should be involved,
where available, for specific treatment and investigations.
• Teach relatives good nursing care/manual handling techniques prior
to discharge home.
 DIFFERENTIAL DIAGNOSIS
• Syncope.
• Encephalitis e.g. due to HIV, toxoplasmosis etc.
• Space occupying lesions(Neoplasm or Infectious): Brain tumours or brain abscess.
• Acute disseminated encephalomyelitis (ADEM) due to demyelination
• Infections and infestations:
-Malaria.
-Cerebral cysticercosis.
-Tuberculous meningitis.
-Cryptococcal meningitis.
• Transient global amnesia (TGA).
• Head injury/Trauma i.e. subdural haematoma or epidural hematoma),
• Hysterical conversion and other psychiatric illness.
• hypo/hyperglycemia, electrolyte abnormalities (e.g. hypo/hypernatremia)
COMPLICATIONS
• Aspiration pneumonia
• Malnutrition
• DVT
• Pulmonary Embolism
• Decubitus ulcer
• Contractures
• Joint abnormalities
• Dehydration
• UTI
• Electrolyte imbalnce
• Other complication related to the area of the brain that has been
damaged
• Damaged to the temporoparietal area-inability to interpret sensory
information
• Damaged to the dominant hemisphere (usually left) produces
problems with speech and language
• Damaged to the nondominant hemisphere (usually right) produce
problems with spatial relationships,the resulting deficits include
agnosia, apraxia, and visual field defects
CONCLUSION

The outcome of
rehabilitation of a CVA will be
different for each patient in
areas of deficit and in the
amount of recovery. Some
patients will recover completely
from the affects of a CVA.
Prevention
• Control of hypertension. .
• Control diabetes mellitus.
• Cessation of cigarette smoking.
• Moderate intake of alcohol increases HDL,
which clears LDL from the circulation into the
liver.
• Oestrogen replacement therapy has been
found to associate with a reduced risk of
subarachnoid haemorrhage in post-
menopausal women.
Cont….
• Increasing physical activity levels of sedentary • It reduces raised blood pressure.
parsons by 30-40 minutes exercise 3 times • It raises the high-density lipoprotein
per week is enough: (HDL) cholesterol and lowers the low
• It promotes weight loss. density lipoprotein (LDL) cholesterol.
• It improves glucose tolerance. • It promotes lifestyle conducive to
favourably changing detrimental health
habits such as cigarette smoking
Cont….
Health education:
• Educate the public to raise awareness of
stroke prevention.
• Educate health care providers on:
-The need for rapid response.
-Preventable nature of stroke.
-Warning symptoms of the disease.
Case
• A 49 yo woman developed a throbbing headache that lasted for
approximately 30 minutes and then slowly faded away. Similar
headaches occurred occasionally for the next week. One day as she
was lifting a heavy chair, she experienced a sudden, severe headache
that was accompanied by nausea, vomiting, and general feeling of
weakness. She decided to see her physician immediately.
• Physician detected neck stiffness, elevated BP. Her deep tendon
reflexes were symmetrical and all modalities of sensation were
normal
CONT….
• What is a provisional diagnosis?
• What are investigation should be done?
CONT…
• Provisional Diagnosis is Sub arachnoid hemorrhage (SAH)
• Investigations
CT Brain scan
Lumbar puncture
Fundoscopy
• Results
CT Brain scan showed –a large saccular aneurysm of the anterior
communicating artery.
The CSF is grossly bloody after centrifugation, the supernatant fluid
was xanthochromatic (yellow-colored).
Visualization of the optic fundus through an ophthalmoscope showed
subhyaloid hemorrhages (bleeding between the retina and vitreous
body)
CONT…
• Diagnosis –Ruptured aneurysm of the anterior communicating artery
and Sub arachnoid hemorrhage (SAH)
Case 1 A 65 yo M is brought in by his family after he was noted to have left sided weakness and slurring of
his words. 1. What is your impression? 2. What is the definition of stroke? 3. What are the risk factors for
stroke (which you would ask about)? 4. What is the most likely type of stroke in this patient? 5. What are
the types of ischemic stroke? 6. What differential diagnoses would you consider?
The patient and his family are unsure but they think the symptoms began about 24 hours ago. The patient
denies any fever, headache or changes in his vision. He does not have any chest pain or dyspnea. Past
medical history is significant for HTN and DM. On exam he is afebrile with a BP of 170/90 and HR 85. He is
awake and alert and following commands. He has a left facial droop and is mildly dysarthric. He has 5/5
strength on his right but 3+/5 strength on his left upper extremities and 4/5 strength in his left lower
extremities. Sensation is intact. Reflexes are brisk but symmetric. He has no meningeal signs. Fundoscopic
exam reveals no papilledema. Cardiac exam is normal. He has no carotid bruits. Lungs are clear.
7. What investigations do you want to order? 8. What part of the brain is effected?
You admit the pt. to the ICU. You order a FBP, creatinine, RBG, lipid panel, EKG and noncontrast head CT.
While you think that the patient likely had an embolic stroke you hold off on starting ASA until you can
rule out a hemorrhagic stroke definitively with the CT scan. You decide to keep the blood pressure as is.
The patient’s RBG is 9.3. The EKG reveals LAD and LVH but no ischemic changes. The CT results return and
are consistent with an ischemic lacunar infarct of the right internal capsule and also involving the right
lobe. The rest of the labs are pendingy9. What is the most likely etiology of ischemic stroke in this patient?
10. What treatments will you initiate? . You start the patient on ASA, simvastatin, ranitidine and sub-q
heparin. You order the patient for physical therapy. The rest of the patient’s labs return back normal. The
patient’s speech and strength begin to improve after several days in the ICU and he shows no signs of
increased ICP. You decide to transfer the patient to the floor with plans to eventually start him on
Case 2 A 42 yo F with HTN is brought in by her family after a witnessed collapse and loss of
consciousness that occurred 6 hours ago. Just before collapsing the patient had complained
of headache. She vomited once, and then collapsed. She has no other medical problems
and is not on any medications.
1. What is your impression? 2. What type of stroke does this patient likely have? 3. What
are the 2 kinds of hemorrhagic stroke? 4. What risk factors would you ask about for
this type of stroke? The patient is brought to the ICU. On exam she is afebrile, her BP is
190/100, HR 85. She is unconscious and does not open her eyes to voice. She
occasionally moans. Pressure on her nailbed elicits flexion of her arm. Her neck is stiff.
Pupils are equal, round and reactive. Fundoscopic exam does not reveal papilledema.
Heart and lungs are clear. You order a FBP, creatinine, rapid test, lipid panel, EKG. You
are informed by your chief that the CT scanner is not working.
5. What is the patient’s GCS? 6. How do you want to treat this patient? You calculate the
pt’s GCS as 6. You suspect that the patient had a subarachnoid hemorrhage. You decide to
treat her with IV hydralazine to bring her blood pressure down and also start nimodipine
and phenytoin. You perform an LP to rule out meningitis (although it is lower on your
differential) and to check for xanthochromia. EKG reveals deep T-wave inversions in all
leads. Her labs are all normal and her rapid test is negative. You continue to monitor the
patient in the ICU and after several days the patient’s GCS begins to improve.
Epilepsy and
Status
Epilepticus
Outline of the Course
• Introduction
• Pathophysiology
• Aetiology
• Classification
• Investigations
• Treatment
• Status Epilepticus
Introduction
• Seizure is an abnormal electrical discharge in the brain that results in
a sudden change in behavior, sensory perception or motor activity.
• Epilepsy refers to recurrent, unprovoked seizures from known or
unknown causes.
• Patient must have 2 or more unprovoked seizure with interval of at
least 24 hours apart to be diagnosed with epilepsy.
• A recent change in definition allows the diagnosis of epilepsy to be
made after a single seizure with a high risk of recurrence (e.g. a single
seizure in the presence of a cortical lesion.
Introduction
• The term ‘ictus’ describes the period in which the
seizure occur, and ‘post ictal’ describe the period of
which the seizure has ended but before the patient
has returned to his or her baseline mental status.
• Convulsion; A medical condition characterized by
involuntary repetitive contraction and relaxation of
body muscles leading to abnormal movements of
the body.
• Febrile convulsion; seizures that occur in children
aged 6 month to 6 years in response to extra cranial
infection.
Pathophysiology
• Seizure occur because of biochemical imbalance between excitatory
neurotransmitters( Glutamate ) and inhibitory force ( GABA) at the
neuronal cell membrane.
• The biochemical imbalance results in repeated, abnormal electrical
discharges that may stay within certain area of the brain(Focal), or
may propagate through out the brain resulting in generalized seizure.
• Seizure also produce number of physiologic changes; transient
hypoxia, transient hyperthermia, hyperglycemia and lactic acidosis.
Aetiological factors
• The common causes of seizures in infants and children include:
Congenital malformations
Prenatal injuries or hypoxia
Developmental neurologic disorders
Metabolic defects
Head Injuries
Infections
Count;
• In young adults seizures are commonly caused by
Head trauma
Brain tumors
Infection/high fever
Arteriovenous malformations
• In elderly seizures may be caused by
Cerebrovascular disease
CNS degenerative diseases
Brain tumors are common causes
Genetic risk increases 2-3 times in individuals with first degree relatives suffering
epilepsy
Head trauma
Count;
• Precipitating factors of seizures are
Sleep deprivation
Emotional disturbances/stress
Flickering light like in discos, or after watching TV over many hours
Poor drug compliance
Medical drugs such as Chlorpromazine, Haloperidol are safer but can still
cause fits in high doses
Alcohol and drugs like Amphetamine and Cocaine
Hypoglycemia
Classification of seizures
• Seizures are described and distinguished by clinical pattern as
• Focal Seizures - beginning focally in one area of the brain
• Generalized Seizures - They start generalized (bilateral) in the whole brain at
the same time.
 Classification Seizures

• Focal or partial seizure; localized to the area of origin and have signs
and symptoms referable to the part of hemisphere.
Simple partial seizures
Complex partial seizures
Partial seizures with secondary generalization
• Generalized seizures; originate in centrally positioned cells and
activate all parts of the brain simultaneously leading to reduced level
of consciousness.
Absence seizure, Tonic-clonic seizure, Myoclonic seizure, atonic seizure
Generalized seizures
• Tonic–clonic seizures(formerly wrongly called Grand Mal)
• An initial ‘aura’ may be experienced by a pt. depending on the region of brain
affected,
• The patient then becomes rigid (tonic) and unconscious, falling heavily if
standing (‘like a log’). During this phase, breathing stops and central cyanosis
may occur.
• During the attack, urinary incontinence and tongue-biting may occur
• Then a patient enter into a Jerking (clonic) movements which emerge for 2
minutes at most.
• In the Post-ictal phase the patient can be in deep coma with Todd’s paralysis.
Generalized seizures
• Absence seizures
• Absence seizures (previously ‘petit mal’) always start in childhood.
• Starts suddenly without aura
• Lasts for some seconds only
• Patient does not fall down
• Loss of awareness, patient stares , seems absent minded, stops talking
or responding
• Regains consciousness suddenly without post-ictal abnormalities and
continues his activities as if nothing happened
Generalized seizures
• Myoclonic seizures These are typically brief, jerking movements,
predominating in the arms.
• Atonic seizures These are seizures involving brief loss of muscle tone,
usually resulting in heavy falls with or without loss of consciousness.
Focal seizures
• Simple partial seizures with motoric fits of some part of the body but
no loss of consciousness and frequently with aura
• Complex partial seizures with reduced level of consciousness and
frequently with aura
• Partial seizures with secondary generalization. These begin as simple
or complex partial seizures but then spread to the rest of the brain
and look like generalized tonic-clonic seizures with movements and
frequently with aura,
• An aura represents the initial phase of a focal seizure
Differential Diagnosis
 Pyrexia (fever),Cerebral Malaria
o Convulsions occuring in children under 5 years due to high grade fever known as febrile convulsions .In
the majority there is no recurrence,Febrile convulsions are not usually labeled as epilepsy
• Brain tumors and abscesses :Mass occupying lesions (SOL) in the cortex cause seizure either partial or
secondary generalized seizures ,Hydrocephalus also lowers seizures threshold
• Vascular problems :Seizures sometimes follow cerebral infarction especially in the elderly;There is a
peak in incidence late in life ;May present with seizures and occasionally a subarachnoid bleeding
• Alcohol, drugs and drug withdrawal: Chronic alcohol abuse is a common cause of seizures,Occurs either
while drinking heavily (rum fit) or during periods of withdrawal ,Alcohol-induced hypoglycaemia also
provokes epileptiform attacks
o Antipsychotics such as phenothiazides and antidepressants (tricyclics) may sometimes precipitate
epileptic seizures ,Withdrawal of anticonvulsant drugs especially phenobarbitone and benzodiazepines
may provoke seizures,Many medications can lower seizure threshholds (e.g. efavirenz, bupropion)
• Encephalitis and inflammatory conditions
o Seizures occur frequently as presenting features of ƒ Viral encephalitis ƒ Central nervous HIV
manifestations ƒ Toxoplasmosis ƒ Cytomegalovirus ƒ Bacterial and viral meningitis ƒ Neurosyphilis ƒ CNS
cysticercosis (due to calcification by taenia solium cysticerci in the brain) ƒ Cryptococcus meningitis
Metabolic abnormalities
o Seizures are seen with
ƒ Hypocalcaemia ƒ Acute hypoxia ƒ Uraemia ƒ Hepatocellular failure ƒ Hypo or
hypernatremia ƒ Hypoglycemia
• Degenerative brain disorders
o Seizures can occur in dementia like in alzheimer’s disease
• Psychogenic
o Seizures which are mimicking epilepsy may occur in hysteria and other dissociative
disorders
• Pueperal
o Spontaneous paroxysmal muscular contractions and relaxation in postpartum
woman may mimic epilepsy.
• Eclampsia
o Seizures may occur in third trimester pregnancy with hypertension and
glomerulonephritis.
Investigations
• Investigations Done in Primary Health Care Facilities
Blood slides for malaria parasites
FBP (HB is necessary)
Urinalysis (albumin is necessary)
Serological test of HIV after counseling
Blood sugar
Investigations
• Investigations Done in Hospitals (in Addition to those Done in
Primary Health Care Levels)
 Renal (Kidney) function test (serum creatinine or urea)
VDRL (serological test for syphilis)
Serum electrolytes (Na+ K+ Ca2+ )
Lumbar puncture (CSF sugar, protein, gram stain, and ZN stain, Indian Ink
stain)
Investigations
• Investigations Done in a Consultant Hospitals (in Addition to those
Done in Other Hospitals)
Brain scan ( CT and MRI)
Electroencephalogram EEG
Electrocardiogram
Management;
• The decision to start treatment should be made in consultation with
the patient and his or her family. And involve proper counselling and
patient education.
• Patient should be warned not to drive and avoid swimming.
• Also discuss occupational hazards e.g. working at heights, using
power tools, etc.
 Treatment approaches
• During a Generalized Tonic-clonic seizure
• Prevent person from hurting himself or herself
• Place something soft under the head
• Loosen tight clothing
• Clear area for sharp or hard objectss
• Do not force any objects into patient's mouth
• Do not restrain patient's movements
• Turn patient on left lateral position to allow saliva to drain from mouth and
avoid aspiration
• Stay with the patient until seizure ends naturally
• Do not pour liquids into patient's mouth or offer any food, drink or medication
until she/he is fully awake
 Mx
Give artificial respiration if patient does not resume breathing after seizure
• Provide area for patient to rest until fully awakened accompanied by responsible person
• Be reassuring and supportive when consciousness returns
• Convulsive seizure (due to epilepsy) is not usually a medical emergency but presence of
any of the following signs indicate the need for immediate medical attention
• Seizure lasting longer than 10 minutes or occurrence of second seizure
• Difficulty in rousing at 20-minute intervals
• Complaints of difficulty with vision
• Vomiting
• Persistent headache after a rest period
o Unconsciousness
o Unequal size pupils or excessively dilated
o Other co-morbid conditions (like abnormal breathing, frothing, unusual smell from the
mouth like rotten fish smell)
Anti-Epileptic Drugs(AEDs)
• The aim of drug treatment is to make the patient seizure free.
• The choice of drug is determined mainly by the type of epilepsy.
• Every effort should be made early on to find the single best drug
(monotherapy) available using the smallest dose with the fewest side
effects
Drug Main indications Dosage Dosage Main side effects
starting maintenance
Phenobarbitone all epilepsies 60 mg/po/daily 180 mg/daily sedation, ataxia,
photosensitivity,
cognitive/behavioural
dysfunction
Carbamazepine partial onset epilepsies 100 mg/po/bd 2–800 mg/bd ataxia/sedation (dose
dependent), rash,
allergic reaction

Phenytoin partial onset/secondary 200–300 mg/po/nocte 3–450 mg/daily ataxia, drowsiness,

generalized seizures dizziness (dose
dependent) hirsutism,
gum hypertrophy,
facial skin thickening
and acne

Sodium Valproate primary generalized 200 mg/po/bd 400–1400 mg/bd nausea, vomiting,
and partial onset tremor, weight gain,
epilepsies hair loss, polycystic
ovary syndrome,
hepatotoxicity,
teratogenesis (dose
dependent),

Ethosuxamide absence seizures only 250 mg/po/od 250–750 mg/bd nausea, drowsiness,
headache, ataxia,
blood dyscrasia
Anti-Epileptic Drugs(AEDs)
• Phenobarbital; first choice for partial and generalized tonic-clonic
seizure initial dose 30 -60mg per day in adults, max dose 180mg per
day.
• Carbamazepine; Reserved for partial seizure, first choice in tonic-
clonic with association with partial seizure; initial dose 100mg bd to
600mg bd.
• Sodium valproate; first choice for generalized seizure, initial dose
300mg bd to 750mg bd.
• Phenytoin; for Tonic-clonic and partial seizure ( 200-500mg per day )
Discontinuing of AEDs
• AEDs may be effectively withdrawn in some patients who have been
seizure free for 2-5 years
• There is an increased risk of recurrence in adults particularly
between 1 and 2 years after stopping.
• Children who have been seizure free for 2 years off medication tend
to remain so.
 AEDs AND WOMEN
• Doubling the dose of COCs
• The use of AEDs in women with epilepsy is associated with increased risk
of teratogenicity .
• Best practice is to use a single drug in the lowest effective dose and to
offer folic acid prophylaxis before conception.
Principles of Treating Epilepsy(module notes//use STG Notes)
• Treat underlying cause • Control the seizures with Phenobarbital • Initial
dose of Phenobarbital for children is 3 - 4 mg/kg once daily or in 2 divided
doses, increase to 8 mg/kg/day if necessary • In adults – in acute seizures,
dilute the injection in 1ml of water for injection, give 10mg/kg at a rate of
not more than 100mg/minute (maximum total dose is 1g). Maintenance
dose is 60-200mg per day.
 STATUS
EPILEPTICUS
Status epilepticus
• Current definition; Prolonged continuous seizure of at least
15minutes or 2 or more discrete seizure attack without regaining
consciousness.
• It is a medical emergency with a mortality rate of 10-20% in Africa.
• The most common cause are;
• Acute CNS infection especially in children.
• Head injury
• Known epilepsy
• Poisoning e.g. pesticide
• Eclampsia and stroke
Management;
Principles of management;
• Remove the patient from potential danger
• ABC
• Stop seizure quickly
• Prevent complications
• Find and control the underlying cause
Management
• Secure the airway with adequate oxygenation (> 95% oxygen
saturation) and ensuring an adequate circulation (pulse & BP) and
establishing iv access .
• A blood glucose should be checked and if low (<3.5 mmol/L) treated
with 50 ml of 50% glucose.
• Give thiamine 100-250 mg by slow IV infusion over 20 minute if
alcoholic or malnourished.
 Support ABCs

First Line Management

ADULTS:
IV DIAZEPAM 5-10mg stat slow IV push, repeat every 5min up to 3 doses as needed
OR
IV MIDAZOLAM 5-10mg slow IV push, repeat every 5min up to 3 doses as needed

Second Line Management

ADULTS:
IV PHENYTOIN 20mg/kg IV slowly (NOT MORE THAN 50mg/min)
OR
IV PHENOBARBITONE 20mg/kg IV slowly (NOT MORE THAN 50mg/min)
Important points to elicit in the
history;
• Events before the seizure;
• An aura or warning or abnormal behavior before the attack suggest focal
origin
• Movement of the head ( localizing sign)
• Reduced consciousness; indicate generalized seizure
• Stiffening ( tonic) or jerking ( clonic or convulsive)
• Tongue biting and incontinence rarely feces
• Post-ictal confusion, drowsiness, or headache
END
Approach to Seizure and Status
Epilepticus(STG)
Status epilepticus
is a single seizure ≥5 minutes in length or two or more seizures without
recovery of consciousness between seizures.
Status epilepticus is a neurologic emergency, and treatment should be
initiated in all patients with continuous seizure activity lasting more than 5
minutes.
Clinical presentations
• Abrupt onset seizures
• Altered mental status
• Postictal drowsiness
• Tongue biting
Differential diagnoses
Epilepsy, meningitis, encephalitis, malaria, space occupying lesion, alcohol withdrawal,
isoniazid toxicity, intracranial hemorrhage, metabolic abnormalities- hyponatremia,
eclampsia, acute hydrocephalus.
Investigations: Blood Glucose, Electrolytes: (Sodium, Potassium, Chloride, Magnesium
and Calcium), ECG, Bedside ultrasound, Blood gases, Malaria Test, Serum creatinine and
urea, Lactate levels, Pregnancy test (females), Toxicology screening and/orCT Head
Non-pharmacological management
• Protect patient from injury (If possible place in left lateral position to reduce
aspiration risks), Don’t place tongue depressor
• Perform both primary and secondary assessment and provide necessary
interventions
• Give Oxygen if needed
• Do bedside random blood sugar test
• Establish IV access for administration of anticonvulsants, if unable use the rectal route
• Connect the patient to the cardiac monitor to obtain vital signs
PHARMACOLOGICAL MANAGEMENT
I. Active seizure 0-5minutes
Supportive care: IV access, monitors, maintain airway, oxygen therapy. Check point-of-care glucose and
provide:
A: dextrose 5%(IV); if glucose is ≤ 3.5mmol/L AND A: diazepam (IV) 0.15-0.2mg/kg. Maximum 10mg
(Rectal dose: 0.2-0.5mg/kg) repeat every 5 minutes up to 3 doses OR
D: midazolam (IV): 0.1mg/kg repeat every 5 minutes up to 3 doses
II. Established Status Epilepticus 5-10 min
B: phenobarbitone (IV): Adults 20mg/kg slowly (max 50mg/min); Paediatrics 20mg/kg slowly (max
30mg/min) OR
C: phenytoin (IV) Adults 20mg/kg slowly (max 50mg/min); Paediatrics 20mg/kg slowly (max 30mg/min)
Consider INTUBATION if patient still seizing
C: thiopental (IV): Adult 3-6mg/kg loading dose then 25-100mg infusion as needed; Paediatrics
2-5mg/kg loading dose OR
D: propofol (IV): Adults 2mg/kg loading dose then 2-10mg/kg/hour; Paediatrics 3mg/kg loading dose,
then 7.5-18mg/kg/hr OR
D: midazolam (IV): Adult 0.2mg/kg loading dose then 0.1-0.2mg/kg/hour; Paediatrics 0.1mg/kg then
infusion 0.06 – 0.4mg/kg/hour
Disposition:Intensive care unit admission or refer to the higher health facility with ICU/HDU capacity
 8.3 Management of
Epilepsy(STG)
Epilepsy
is a common neurological disorder characterised by recurring seizures. About two-thirds of people with
active epilepsy have their epilepsy controlled satisfactorily with anti-epileptic drugs (AEDs).
Other treatment approaches may include surgery and neuromodulation. Optimal management is
required to improve patient’s health outcomes and minimise detrimental impacts on social,
educational, and occupational activities.
Clinical presentation Recurrent seizures
Investigations
• Serum electrolytes
• Serum antiepileptic drug levels
• Electroencephalogram (EEG)
• Brain CT scan
• Brain MRI with epilepsy protocol
Classification of epileptic syndromes Classify epileptic seizures and epilepsy syndromes in all patients
using a multi-axial diagnostic scheme (refer to ILAE classification) as failure to classify the epilepsy
syndrome correctly can lead to inappropriate treatment and persistence of seizures.
Pharmacological management
• Utilize a single AED (monotherapy) and increase dose until seizures are controlled or side
effects cannot be tolerated.
• If the initial treatment is unsuccessful, initiate alternative monotherapy with different drugs
before resorting to drug combinations.
• Combination therapy (adjunctive or 'add-on' therapy) should only be considered when
attempts at monotherapy with AEDs have not resulted in seizure freedom.
• If trials of combination therapy do not bring about worthwhile benefits, revert treatment to
the initial monotherapy regimen that has proved most acceptable to the patient and consider
referral for expert evaluation.
For management of status epilepticus—refer to emergency and critical care chapter
I. Focal seizures
First Line: A: carbamazepine (PO) 10-20mg/kg 12hourly for 4weeks OR
S: lamotrigine (PO) 1-5mg/kg 12hourly for 4weeks
Second line: S: levetiracetam (PO) 10mg/kg 12hourly for 4weeks
Add-on treatment: gabapentin or sodium valproate as adjunctive treatment if first-line
treatments are ineffective or not tolerated.
II. Generalised tonic–clonic (GTC) seizures
C: sodium valproate (PO) 10-15mg/kg 12hourly for 4weeks OR
S: lamotrigine (PO) 1-5mg/kg 12hourly for 4weeks
Add on treatment: offer levetiracetam as adjunctive treatment if first-line
treatments are ineffective or not tolerated.
III. Absence seizures
First Line: C: sodium valproate (PO) 10-15mg/kg 12hourly for 4weeks
Second line: consider levetiracetam
Note DO NOT offer carbamazepine, phenytoin or pregabalin for absence
seizures
IV. Myoclonic seizures
First Line: C: sodium valproate (PO) 10-15mg/kg 12hourly for 4weeks Second
line: S: levetiracetam (PO) 10mg/kg 12hourly for 4weeks
Idiopathic generalised epilepsy (IGE)
First Line: C: sodium valproate (PO) 10-15mg/kg 12hourly for
4weeks Second line: S: lamotrigine (PO) 1-5mg/kg 12hourly for
4weeks
Juvenile Myoclonic epilepsy (JME)
First line: C: sodium valproate (PO) 10-15mg/kg 12hourly for 4weeks
Second line: S: lamotrigine (PO) 1-5mg/kg 12hourly for 4weeks OR
S: levetiracetam (PO) 10mg/kg 12hourly for 4weeks
Childhood absence epilepsy
First Line: C: sodium valproate (PO) 10-15mg/kg 12hourly for
4weeks Second line: S: lamotrigine (PO) 1-5mg/kg 12hourly for
4weeks Add-on treatment: consider clonazepam, levetiracetam if
first-line treatments are ineffective or not tolerated.
Management of epilepsy in pregnancy
The use of antiepileptic drugs (AEDs) is associated with increased baseline risk of fetal
malformations during pregnancy.
Prescribe Folic acid to all women of childbearing age and girls on AEDs preconception.
Attempt to decrease pharmacological treatment to monotherapy and utilize the lowest possible
effective dose of drugs that have shown minimal risk of maternal and fetal neural tube defects
S: lamotrigine (PO) 1-5mg/kg 12hourly for 4weeks OR
S: levetiracetam (PO) 10mg/kg 12hourly for 4weeks AND
A: folic acid (PO) 5mg 24hourly for 3-6months
In women who have not had a seizure for at least 2years, attempt complete withdrawal of AEDs.
Non-pharmacological Treatment
• Consider ketogenic diet—based on specialist assessment and expert opinion
• Refer all medically refractory seizures for expert neurosurgical evaluation for epilepsy surgeries
• Consider evaluation for Vagus Nerve Stimulation (VNS) as an adjunctive treatment in reducing the
frequency of seizures in adults who are refractory to AEDs but who are not suitable for resective
surgery
EPILEPSY
• WHO defines epilepsy as two or more unprovoked seizures . Seizures
in epilepsy occur in absence of specific provocation such as fever,
electrolyte imbalances, or trauma or acute cerebral insults.
• The word seizure describes an involuntary violent spasm, or a series
of jerking of the face, trunk, or extremities with or without loss of
consciousness, sensory, autonomic or behavioral disturbances.
 EPIDEMIOLOGY
• Slightly higher among males than females
• Age of onset: any point in life from Infancy, childhood, adolescence and
adulthood
• More likely to occur in young children, or people over the age of 65 years
• Epilepsy is estimated to affect 0.5-4% of the population around the world.
• The prevalence is said to be higher in developing countries.
• Grand mal seizure account for 40 to 80 %of all types of epileptic seizures.
• •It is estimated that 5-10 % of the population will have at least one seizure
attack in their life time, with the highest incidence occurring in early
childhood and late adulthood.
 ETIOLOGY
• Idiopathic or cryptogenic: in which the cause is unknown, accounts for the majority.
• Genetic factor (Family History)
• Perinatal causes: perinatal asphyxia, birth trauma, perinatal infection
• CNS infections: encephalitis, toxoplasmosis, cerebral malaria,
• Head trauma: penetrating head injury, depressed skull fracture, intracranial hemorrhage and
prolonged post traumatic coma are associated with increased risk of having seizure disorder.
• Neoplasms: metastatic or primary brain tumors
• Vascular causes: Infarction or stroke, vascular malformations
• Metabolic abnormalities: hyponatremia, hypo or hyperglycemia, Uremia ,hypocalcemia
• Inflammatory causes: Systemic lupus erythromatus
• Degenerative diseases: Alzheimer’s disease
• Drugs: Cocaine
 ETIOLOGY OF SEIZURES
Neonatal Period Adolescence and adulthood
• hypoxic ischemic encephalopathy • CNS lesion
• central nervous system (CNS) infections • Idiopathic epilepsy (less common)
• trauma • trauma,
• CNS infections, brain tumors, illicit drug use
• congenital CNS abnormalities
and alcohol withdrawal.
• Metabolic diseases • Hypoglycemia
Late infancy and Early childhood Older adult
• Febrile seizures (fairly common), • cerebrovascular disease (very common cause)
• caused by CNS infections and trauma. • CNS tumors
Childhood • head trauma,
well-defined epilepsy syndromes • Degenerative diseases e.g. dementia
Precipitating factors of seizures are

• Sleep deprivation/disturbance
• Emotional disturbances/stress
• Flickering light like in discos, or after watching TV over many hours
• Poor drug compliance
• Medical drugs such as Chlorpromazine, Haloperidol are safer but can still
cause fits in high doses
• Alcohol and drugs like Amphetamine and Cocaine
• Hypoglycemia
• Fever
• Skipping meals/overeating.
Frequency of fits arising from different
sources
• Temporal lobe 30%
• Frontal lobe 5%
• Parietal lobe 2%
• Occipital lobe 1%
• Primary generalized 13%
• Unlocalized 49%
PATHOGENESIS OF EPILEPSY
• The exact mechanism is not known. However it could be caused by:
• Increased excitability of excitory neurons.
• Down regulation of inhibitory circuits in the brain.
Clinical Classification of seizure.

• Seizures are described and distinguished by clinical pattern as

Partial/Focal Seizures - beginning focally in one area of the brain
 Generalized Seizures - They start generalized (bilateral) in the whole
brain at the same time
Types of Partial/Focal Seizures

 Simple partial seizures involves fits of some part of the body but no
loss of consciousness and frequently with aura
 Complex partial seizures with loss/reduced level of consciousness
and frequently with aura
 Partial seizures with secondary generalization. These begin as
simple or complex partial seizures but then spread to the rest of the
brain and look like generalized tonic-clonic seizures with movements
and frequently with aura
 An aura represents the initial phase of a focal seizure
Types of Primary Generalized
Seizure
Grand Mal Tonic-Clonic Seizure
• Grand mal is a French word meaning the ‘big evil’
• The most common seizure during which the person fall to the ground
• There is sudden loss of consciousness without aura
• Tonic and clonic phase of convulsions ( stiffening of the body, shaking,
loss of bladder or bowel control, biting of the tongue, eye rolling).
• Terminal sleep which lasts for minutes to one hour
• In the post-ictal phase, the child might be hypotonic. Irritability and
headache are common as the child awakens
 Absence Seizure (petit mal)
• Absence or Petit mal a French word meaning ‘small evil’
• Starts suddenly without aura
• Lasts for some seconds only
• Patient does not fall down
• Loss of awareness, seems absent minded, stops talking or responding
• Regains consciousness suddenly without post-ictal abnormalities and
continues his activities as if nothing happened
Other Types of Primary Generalized Seizures
Myoclonic seizure spontaneous quick twitching of the arms and legs
Atonic seizure loss of muscle control and makes patient fall down
suddenly.
 Tonic seizure causes muscle stiffness
Clonic seizure characterized by repeated, jerky muscle movement of
the face, neck and arms.
CLINICAL PRESENTATION
• The clinical signs and symptoms of seizures depend on the location of
the epileptic discharges in the cerebral cortex and the extent and
pattern of the propagation of the epileptic discharge in the brain.
Information is obtained from both the patient and witness of the event.
The following should be enquired:
• Was there any warning signs before the ictal phase: this is known as
aura. Aura is common in epilepsy. During aura a patient may
experience perception of a strange light, an unpleasant smell, or
confusing thoughts or experiences or hallucinations.
• When occurring, auras allow some people who have epilepsy time to
prevent injury to themselves and/or others.
• What is events occurred during the ictal phase: these is very
important as it can determine the type of seizure the patient
experienced. It include the following:
• Which limbs where involved
• Ask if there was tongue biting, eye rolling, fecal or urinary
incontinence, froth in the mouth.
• Ask the duration of the attack
• Ask the number of attacks and if there was regaining consciousness
between the attacks.
• What events occurred after the attack( post ictal events):
• Confusion
• Extreme fatigue
• Memory Loss
• Drowsiness
• Nausea
• Headache/migraine
• psychosis
• Poor attention and concentration
• Depression
Physical examination
• For patients who for years have had intractable generalized tonic-
clonic seizures are likely to have suffered injuries requiring stitches.
• Do a full neurological assessment of the patient
INVESTIGATION IN EPILEPSY
• EEG- abnormal electrical activity in the brain.
• Imaging such as MRI and CT scan, they are not required routinely for
childhood epilepsy.
• They can be used to identify tumour, vascular lesion in the brain.
• Other investigations includes blood test for example RBG, serum
sodium, calcium and potassium, lumbar puncture.
 TREATMENT OF EPILEPSY
• The goal of treatment in patients with epileptic seizures is to achieve a
seizure-free status without adverse effects.
• Treat underlying cause, avoid triggers.
• Monotherapy (starting with one drug) is usually preferred as it is cheaper
with less side effects and less drug interactions. The drug to be used
depends on the pattern of seizure:
• Absence seizures: Give Ethosuximide PO 2.5mg/kg 12 hourly increase
gradually over 2 weeks to a maintenance dose of 20 mg/kg/day (max 1
g/day)
• Myoclonic epilepsy: give sodium valproate PO 5mg/kg 12 hourly increase
gradually by 5mg/kg every 2 weeks to a maximum of 30 mg/kg/day.
• Generalized epilepsy: Sodium valproate PO 5mg/kg 12 hourly
increase gradually by 5mg/kg every 2 weeks to a maximum of 30
mg/kg/day if no seizure control add carbamazepine PO 2.5mg/kg 12
hourly, increase gradually every 2 weeks by 2.5mg/kg 12 hourly to a
maximum dose of 10mg/kg 12hourly.
• Focal epilepsy: Give Carbamazepine PO 2.5mg/kg 12 hourly, increase
gradually every 2 weeks by 2.5mg/kg 12 hourly to a maximum dose of
10mg/kg 12hourly OR
Give Lamotrigine PO 0.15mg/kg 12 hourly for 2 weeks, then increase
gradually by 0.15mg/kg 12 hourly every 2 weeks to a maximum dose of
10mg/kg/day
IF NO SEIZURE CONTROL
• Give Sodium valproate PO 5mg/kg 12 hourly increase gradually by
5mg/kg every 2 weeks to a maximum of 30 mg/kg/day
 DIFFERENTIAL DIANOSIS

• Pediatric febrile convulsion

• Transient ischemic attacks
• Sleep disorders
• Hydrocephalus
• Brain tumors/ SOL
• Stroke
• Alcohol/drug withdrawal
• Encephalitis
• Metabolic disorder hypo/hyper (glycemia, thermia, calcemia)
• Degenerative disease eg alzheimers disease.
 Complications

• Status epilepticus
• Accidents
• Hypoxic brain damage
• Mental retardation and impairment of intellectual function
• Sudden death
• Psychosocial (Social stigma).
PROGNOSIS
• The patient's prognosis for disability and for a recurrence of epileptic
seizures depends on the type of epileptic seizure and the epileptic
syndrome in question.
• Trauma usually associated with generalized tonic clonic seizures. Such
injuries include ecchymosis; hematomas; abrasions; tongue, facial,
and limb lacerations; burns and even shoulder dislocation
• Impaired level of consciousness is associated with higher morbidity
and mortality.
PATIENT EDUCATION
• To prevent injuries during seizure episodes. This is one of the reasons
for restrictions on driving, swimming, taking unsupervised baths,
working at significant heights, and the use of fire for patients who
have epilepsy
• Educate patients on adherence on medication.
Status epilepticus
• Status epilepticus is a single seizure ≥5 minutes in length or two or
more seizures without recovery of consciousness between
seizures.Status epilepticus is a neurologic emergency, and treatment
should be initiated in all patients with continuous seizure activity lasting
more than 5 minutes.
Etiology
• New-onset epilepsy of any type
• Drug intoxication or drug withdrawal (especially missed
anticonvulsant doses among children with preexisting epilepsy)
• Acute head trauma
• Infection
• Ischemic stroke, intracranial hemorrhage
• Metabolic disorders eg; hypoglycemia, electrolyte imbalance
• Hypoxia
Status Epilepticus Treatment
Time post
onset Treatment
Onset Ensure adequate ventilation/O2
2-3 min. IV line with NS, rapid assessment, blood draw
4-5 min. Lorazepam 4 mg (0.1 mg/kg) or diazepam
10 mg (0.2 mg/kg) over 2 minutes via
second IV line or rectal diazepam
7-8 min. Thiamine 100 mg, 50% glucose 25 mg IV Either
IV phenytoin (15-18mg/kg)-over 60min or fosphenytoin (10-
20mg/kg) is effective
C-Slide 139
 SESSION 27
Diabetes Mellitus
CMT05210 INTERNAL MEDICINE

06/21/2025 140
 Learning Objectives

• By the end of this session, students will be able to:

• Describe diabetes mellitus
• Classify diabetes mellitus
• Describe clinical features and investigations of diabetes
mellitus
• Outline management of diabetes mellitus
• Describe complications of diabetes mellitus

06/21/2025 141
What is diabetes?
 Diabetes mellitus (DM) is a group of diseases
characterized by high levels of blood glucose resulting
from defects in insulin production, insulin action, or both.

 The term diabetes mellitus describes a metabolic

disorder of multiple aetiology characterized by chronic
hyperglycaemia with disturbances of carbohydrate, fat
and protein metabolism resulting from defects in insulin
secretion, insulin action, or both.

 The effects of diabetes mellitus include long–term

damage, dysfunction and failure of various organs.

06/21/2025 142
Diabetes
 Diabetes mellitus may present with characteristic symptoms such as
thirst, polyuria, blurring of vision, and weight loss.

 In its most severe forms, ketoacidosis or a non–ketotic hyperosmolar

state may develop and lead to stupor, coma and, in absence of
effective treatment, death.

 Often symptoms are not severe, or may be absent, and consequently

hyperglycaemia sufficient to cause pathological and functional
changes may be present for a long time before the diagnosis is made.
06/21/2025 143
Diabetes Long-term Effects
 The long–term effects of diabetes mellitus include progressive
development of the specific complications of retinopathy with
potential blindness, nephropathy that may lead to renal failure,
and/or neuropathy with risk of foot ulcers, amputation, Charcot
joints, and features of autonomic dysfunction, including sexual
dysfunction.

 People with diabetes are at increased risk of cardiovascular,

peripheral vascular and cerebrovascular disease.

06/21/2025 144
Burden of Diabetes
 The development of diabetes is projected to reach pandemic
proportions over the next10-20 years.

 International Diabetes Federation (IDF) data indicate that by the

year 2025, the number of people affected will reach 333 million –
90% of these people will have Type 2 diabetes.

 In most Western societies, the overall prevalence has reached 4-

6%, and is as high as 10-12% among 60-70-year-old people.

 The annual health costs caused by diabetes and its complications

account for around 6-12% of all health-care expenditure.

06/21/2025 145
Types of Diabetes
• Type 1 Diabetes Mellitus
• Type 2 Diabetes Mellitus
• Gestational Diabetes

06/21/2025 146
Type 1 diabetes
 Was previously called insulin-dependent diabetes mellitus (IDDM) or juvenile-
onset diabetes.
 Type 1 diabetes develops when the body’s immune system destroys
pancreatic beta cells, the only cells in the body that make the hormone
insulin that regulates blood glucose.
 This form of diabetes usually strikes children and young adults, although
disease onset can occur at any age.
 Type 1 diabetes may account for 5% to 10% of all diagnosed cases of diabetes.
 Risk factors for type 1 diabetes may include autoimmune, genetic, and
environmental factors.

06/21/2025 147
Type 2 diabetes
 Was previously called non-insulin-dependent diabetes mellitus
(NIDDM) or adult-onset diabetes.
 Type 2 diabetes may account for about 90% to 95% of all diagnosed
cases of diabetes.
 It usually begins as insulin resistance, a disorder in which the cells
do not use insulin properly. As the need for insulin rises, the
pancreas gradually loses its ability to produce insulin.
 Type 2 diabetes is associated with older age, obesity, family history
of diabetes, history of gestational diabetes, impaired glucose
metabolism, physical inactivity, and race/ethnicity.
 African Americans, Hispanic/Latino Americans, American Indians,
and some Asian Americans and Native Hawaiians or Other Pacific
Islanders are at particularly high risk for type 2 diabetes.
 Type 2 diabetes is increasingly being diagnosed in children and
06/21/2025
adolescents. 148
Gestational diabetes
 A form of glucose intolerance that is diagnosed in some
women during pregnancy.
 Gestational diabetes occurs more frequently among African
Americans, Hispanic/Latino Americans, and American Indians.
It is also more common among obese women and women
with a family history of diabetes.
 During pregnancy, gestational diabetes requires treatment to
normalize maternal blood glucose levels to avoid
complications in the infant.
 After pregnancy, 5% to 10% of women with gestational
diabetes are found to have type 2 diabetes.
 Women who have had gestational diabetes have a 20% to 50%
chance of developing diabetes in the next 5-10 years.
06/21/2025 149
 Secondary DM
Secondary causes of Diabetes mellitus include:

 Acromegaly,
 Cushing syndrome,
 Thyrotoxicosis,
 Pheochromocytoma
 Chronic pancreatitis,
 Cancer
 Drug induced hyperglycemia:
◦ Atypical Antipsychotics - Alter receptor binding characteristics, leading to increased insulin
resistance.
◦ Beta-blockers - Inhibit insulin secretion.
◦ Calcium Channel Blockers - Inhibits secretion of insulin by interfering with cytosolic calcium
release.
◦ Corticosteroids - Cause peripheral insulin resistance and gluconeogensis.
◦ Fluoroquinolones - Inhibits insulin secretion by blocking ATP sensitive potassium channels.
◦ Naicin - They cause increased insulin resistance due to increased free fatty acid mobilization.
◦ Phenothiazines - Inhibit insulin secretion.
◦ Protease Inhibitors - Inhibit the conversion of proinsulin to insulin.
◦ Thiazide Diuretics - Inhibit insulin secretion due to hypokalemia. They also cause increased
06/21/2025 insulin resistance due to increased free fatty acid mobilization. 150
Pathophysiology of Diabetes

When you eat, your body

breaks food down into
glucose. Glucose is a
type of sugar that is
your body’s
main source
of energy.

6
Pathophysiology of Diabetes

As blood glucose rises, the

body sends a signal to
the pancreas, which
releases insulin.

7
Pathophysiology of Diabetes

Acting as a key, insulin

binds to a place on the
cell wall (an insulin
receptor), unlocking
the cell so glucose can
pass into it. There,
most of the glucose is
used for energy right
away.

7
Blood glucose regulation
Blood glucose
goes up and down
throughout the
day:
 As your blood glucose
rises
(after a meal), the
pancreas releases insulin.

8
Type 2 diabetes
Your pancreas may not
produce enough insulin
(insulin deficiency).

Your cells don’t use

insulin properly.
The insulin can’t
fully “unlock” the
cells to allow
glucose to enter
13 (insulin resistance).
Diagnosis of Diabetes Mellitus

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Values of Diagnosis of Diabetes Mellitus

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Prevention or delay of diabetes:
Life style modification
 Research studies have found that lifestyle changes can prevent
or delay the onset of type 2 diabetes among high-risk adults.

 These studies included people with IGT and other high-risk

characteristics for developing diabetes.

 Lifestyle interventions included diet and moderate-intensity

physical activity (such as walking for 2 1/2 hours each week).

 In the Diabetes Prevention Program, a large prevention study

of people at high risk for diabetes, the development of
diabetes was reduced 58% over 3 years.

06/21/2025 158
Prevention or delay of diabetes: Medications
 Studies have shown that medications have been successful in
preventing diabetes in some population groups.
 In the Diabetes Prevention Program, people treated with the drug
metformin reduced their risk of developing diabetes by 31% over 3
years.
 Treatment with metformin was most effective among younger,
heavier people (those 25-40 years of age who were 50 to 80 pounds
overweight) and less effective among older people and people who
were not as overweight.
 Similarly, in the STOP-NIDDM Trial, treatment of people with IGT with
the drug acarbose reduced the risk of developing diabetes by 25%
over 3 years.
 Other medication studies are ongoing. In addition to preventing
progression from IGT to diabetes, both lifestyle changes and
medication have also been shown to increase the probability of
06/21/2025 reverting from IGT to normal glucose tolerance. 159
 Management of
Diabetes Mellitus

06/21/2025 160
Management of DM
• The major components of the treatment of diabetes
are:

A • Diet and Exercise

• Oral hypoglycaemic
B therapy

C • Insulin Therapy

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A. Diet
 Diet is a basic part of management in every case. Treatment cannot
be effective unless adequate attention is given to ensuring
appropriate nutrition.

 Dietary treatment should aim at:

◦ ensuring weight control
◦ providing nutritional requirements
◦ allowing good glycaemic control with blood glucose levels as close to normal
as possible
◦ correcting any associated blood lipid abnormalities

06/21/2025 162
A. Diet (cont.)
The following principles are recommended as dietary guidelines for people
with diabetes:

 Dietary fat should provide 25-35% of total intake of calories but saturated
fat intake should not exceed 10% of total energy. Cholesterol
consumption should be restricted and limited to 300 mg or less daily.

 Protein intake can range between 10-15% total energy (0.8-1 g/kg of
desirable body weight). Requirements increase for children and during
pregnancy. Protein should be derived from both animal and vegetable
sources.

 Carbohydrates provide 50-60% of total caloric content of the diet.

Carbohydrates should be complex and high in fibre.

 Excessive salt intake is to be avoided. It should be particularly restricted in

06/21/2025 people with hypertension and those with nephropathy. 163
Exercise
 Physical activity promotes weight reduction and improves insulin
sensitivity, thus lowering blood glucose levels.

 Together with dietary treatment, a programme of regular physical

activity and exercise should be considered for each person. Such a
programme must be tailored to the individual’s health status and
fitness.

 People should, however, be educated about the potential risk of

hypoglycaemia and how to avoid it.
06/21/2025 164
B. Oral Anti-Diabetic Agents

• There are currently four classes of oral anti-diabetic agents:

i. Biguanides
ii. Insulin Secretagogues – Sulphonylureas
iii. Insulin Secretagogues – Non-sulphonylureas
iv. α-glucosidase inhibitors
v. Thiazolidinediones (TZDs)

06/21/2025 165
B.1 Oral Agent Monotherapy

 If glycaemic control is not achieved (HbA1c > 6.5%

and/or; FPG > 7.0 mmol/L or; RPG >11.0mmol/L) with
lifestyle modification within 1 –3 months, ORAL ANTI-
DIABETIC AGENT should be initiated.

 In the presence of marked hyperglycaemia in newly

diagnosed symptomatic type 2 diabetes (HbA1c > 8%,
FPG > 11.1 mmol/L, or RPG > 14 mmol/L), oral anti-
diabetic agents can be considered at the outset
together with lifestyle modification.

06/21/2025 166
B.1 Oral Agent Monotherapy (cont.)

As first line therapy:

 Obese type 2 patients, consider use of metformin, acarbose or TZD.

 Non-obese type 2 patients, consider the use of metformin or insulin secretagogues

 Metformin is the drug of choice in overweight/obese patients. TZDs and acarbose

are acceptable alternatives in those who are intolerant to metformin.

 If monotherapy fails, a combination of TZDs, acarbose and metformin is

recommended. If targets are still not achieved, insulin secretagogues may be added
06/21/2025 167
B.2 Combination Oral Agents

Combination oral agents is indicated in:

• Newly diagnosed symptomatic patients with HbA1c >10

• Patients who are not reaching targets after 3 months on monotherapy

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B.3 Combination Oral Agents and Insulin
 If targets have not been reached after optimal dose of combination
therapy for 3 months, consider adding intermediate-acting/long-acting
insulin (BIDS).

 Combination of insulin+ oral anti-diabetic agents (BIDS) has been shown to

improve glycaemic control in those not achieving target despite maximal
combination oral anti-diabetic agents.

 Combining insulin and the following oral anti-diabetic agents has been
shown to be effective in people with type 2 diabetes:
◦ Biguanide (metformin)
◦ Insulin secretagogues (sulphonylureas)
◦ Insulin sensitizers (TZDs)(the combination of a TZD plus insulin is not an approved
indication)
◦ α-glucosidase inhibitor (acarbose)

 Insulin dose can be increased until target FPG is achieved.

06/21/2025 169
 Diabetes
Management
Algorithm

06/21/2025 170
Oral Hypoglycaemic Medications

06/21/2025 171
General Guidelines for Use of Oral Anti-Diabetic Agent inDiabetes
 In elderly non-obese patients, short acting insulin secretagogues can be
started but long acting Sulphonylureas are to be avoided. Renal function
should be monitored.

 Oral anti-diabetic agent s are not recommended for diabetes in pregnancy

 Oral anti-diabetic agents are usually not the first line therapy in diabetes
diagnosed during stress, such as infections. Insulin therapy is recommended
for both the above

 Targets for control are applicable for all age groups. However, in patients with
co-morbidities, targets are individualized

 When indicated, start with a minimal dose of oral anti-diabetic agent, while
reemphasizing diet and physical activity. An appropriate duration of time (2-
16 weeks depending on agents used) between increments should be given to
allow achievement of steady state blood glucose control
06/21/2025 172
C. Insulin Therapy

Short-term use:
 Acute illness, surgery, stress and emergencies
 Pregnancy
 Breast-feeding
 Insulin may be used as initial therapy in type 2 diabetes
 in marked hyperglycaemia
 Severe metabolic decompensation (diabetic ketoacidosis, hyperosmolar nonketotic coma, lactic
acidosis, severe hypertriglyceridaemia)

Long-term use:
 If targets have not been reached after optimal dose of combination therapy or BIDS, consider
change to multi-dose insulin therapy. When initiating this,insulin secretagogues should be
stopped and insulin sensitisers e.g. Metformin or TZDs, can be continued.
06/21/2025 173
Insulin regimens
 The majority of patients will require more than one daily injection if good
glycaemic control is to be achieved. However, a once-daily injection of an
intermediate acting preparation may be effectively used in some patients.

 Twice-daily mixtures of short- and intermediate-acting insulin is a

commonly used regimen.

 In some cases, a mixture of short- and intermediate-acting insulin may be

given in the morning. Further doses of short-acting insulin are given before
lunch and the evening meal and an evening dose of intermediate-acting
insulin is given at bedtime.

 Other regimens based on the same principles may be used.

 A regimen of multiple injections of short-acting insulin before the main

meals, with an appropriate dose of an intermediate-acting insulin given at
bedtime, may be used, particularly when strict glycaemic control is
06/21/2025
mandatory. 174
 Overview of Insulin and Action

06/21/2025 175
06/21/2025 176
Self-Care

 Patients should be educated to practice self-care. This allows the

patient to assume responsibility and control of his / her own diabetes
management. Self-care should include:

◦ Blood glucose monitoring

◦ Body weight monitoring
◦ Foot-care
◦ Personal hygiene
◦ Healthy lifestyle/diet or physical activity
◦ Identify targets for control
◦ Stopping smoking
06/21/2025 177
06/21/2025 178
06/21/2025 179
Diabetes Injection Sites

06/21/2025 180
Diabetes Mellitus
• When rapid acting or short acting insulin is mixed with longer acting
insulin, draw the short acting insulin into the syringe first.
• Prevents contamination of the shorter acting insulin with the longer
acting insulin
• Draw up clear, then cloudy
• Insuling glargine (Lantus) should not be mixed with any other insulin

06/21/2025 181
Diabetes Mellitus
• Mixing insulin

06/21/2025 182
COMPLICATIONS OF DM
 Key Points
• Diabetes mellitus is primarily due to insulin deficiency or
resistance.
• Hyperglycemia is a cardinal manifestation of diabetes mellitus.
• Depending on the etiology of the DM, factors contributing to
hyperglycemia may include
• Reduced insulin secretion
• Decreased glucose usage and
• Increased glucose production
• Diabetic ketoacidosis (DKA) nonketotic hyperosmolar state
(NKHS) and hypoglycemia are acute complications of diabetes

06/21/2025 184
 Evaluation
• Explain the clinical features of DM.
• Describe the treatment of diabetes mellitus.
• Mention chronic complications of diabetes mellitus.
• Explain the importance of health education regarding
the patient of diabetes mellitus

06/21/2025 185
References
• National Diabetes Fact Sheet 2003, DEPARTMENT OF HEALTH AND HUMAN SERVICES Centres for Disease
Control and Prevention

• World Health Organization. Definition, Diagnosis and Classification of Diabetes Mellitus and its
Complications. Report of WHO. Department of Non-communicable Disease Surveillance. Geneva 1999

• Academy of Medicine. Clinical Practice Guidelines. Management of type 2 diabetes mellitus.

MOH/P/PAK/87.04(GU), 2004

• NHS. Diabetes - insulin initiation - University Hospitals of Leicester NHS Trust Working in partnership with
PCTs across Leicestershire and Rutland, May 2008.

06/21/2025 186
 DIABETES MELLITUS (STG)
Diabetes mellitus is a clinical syndrome characterized by persistently high
blood glucose values due to deficiency or diminished effectiveness of
insulin.
Classification Diabetes mellitus
can be classified as follows:
•Type 1 Diabetes Mellitus (T1DM) – due to autoimmune β-cell destruction
• Type 2 Diabetes Mellitus (T2DM) – due to a progressive loss of β-cell
insulin secretion frequently with underlying insulin resistance
• Gestational Diabetes Mellitus (GDM) – diabetes diagnosed in the second
or third trimester of pregnancy that was not clearly overt diabetes prior to
gestation
• Specific types of diabetes – due to other causes e.g., monogenic,
diseases of the exocrine pancreas and drugs or chemicals.
Diagnostic Criteria
• Main clinical features of diabetes are thirst, polydipsia, polyuria, tiredness, loss
of weight, blurring of vision.
• Many people have no classical symptoms and may only present late with the
symptoms related to complications e.g., pruritus vulvae and balanitis due to
infections, paraesthesia or pain in the limbs, non-healing ulcers, and recurrent
bacterial infections
WHO diagnostic Criteria 2006 :Fasting plasma glucose level ≥ 7.0 mmol/L (126
mg/dL) AND Plasma glucose≥ 11.1 mmol/L (200 mg/dL) two hours after a 75 g oral
glucose load in a glucose tolerance test
• Symptoms of hypogycaemia and casual plasma glucose ≥11.1 mmol/L (200
mg/dL)
• Glycatedhemoglobin (HbA1c) ≥ 6.5%.
Diagnosis of gestational diabetes (WHO criteria 2013) :Fasting plasma glucose 5.1–
6.9 mmol/l
• 2–hour plasma glucose 8.5–11.0 mmol/l following a 75g oral glucose load.
At risk screening
Early diagnosis and good control reduce the risk of costly complications and reduces the
deterioration of islet function in T2DM.
The following people should therefore be screened with fasting blood glucose or HbA1c
at least yearly when they visit health facilities: :
• Those aged ≥40 years
• Children and adults less than 40 years who are overweight or obese and who have two
or more additional risk factors of Diabetes Mellitus
• Individuals with impaired glucose tolerance or impaired fasting glucose or a history of
a cardiovascular event
• People on long-term steroids or immunosuppressants
• Women with a history of gestational diabetes mellitus or polycystic ovary syndrome
• All pregnant women at the first antenatal visit if overweight, have had gestational
diabetes, babies with birth weight >4 kg, previous stillbirths or neonatal deaths.
Screening should be repeated in the second trimester if negative.
• All women during the 2nd or 3rd trimester (for gestational diabetes).
Goals for Optimum Management Of Diabetes
• Body Mass Index:Therapeutic goal is 5–10% weight loss for people who are
overweight or obese, but aim for BMI<25kg/m2
• Waist Circumference:<102 cm for men, <88 cm for women
• Physical Activity:At least 30 minutes of moderate physical activity on most days of
the week (total ≥150 minutes/week)
• Blood Glucose Level:Non-pregnant: 4–6 mmol/L fasting; 6–8 mmol/L
postprandial ,Pregnant: ≤5.0 mmol/L fasting, ≤6.7 mmol/L postprandial.Self-
monitoring of blood glucose is essential to improve outcomes
• HbA1c :Target ≤7% (6.5–7.5%). Should be measured every three months until
stable, thereafter at least twice a year
• Blood Pressure:Target ≤140/90 mmHg For those with albuminuria/proteinuria
<130/80 mmHg
• Urine Albumin:Spot collection: <20 mg/L
Urine albumin-to-creatinine ratio (UACR): women: <3.5 mg/mmol; men: <2.5
mg/mmol
 Non-pharmacological Management
Healthy lifestyle
1.Dietary Control:Attain and maintain near normal blood glucose levels to prevent hypo- and
hyperglycaemia and so minimize the onset of chronic complications. Each meal should consist
of a variety of foods from the core food groups (vegetables, fruits, whole grains, meat and
proteins, dairy products)
o Distribute foods evenly throughout the day with small/light meals in between the three
main meals
2.Food composition
Protein: 15-20% of total energy (1g/kg/day),Energy from carbohydrates: 45-60% of total
calories,Less than 100gms carbohydrates per day is not advisable as it
leads to ketosis.The distribution and amount of carbohydrates between meals
should be synchronized with the action of insulin and drugs.
 Distribute the food over three meals with snacks in between rather than 1 or 2 large meals.
Give more of carbohydrate as complex starches e.g. whole grain,cereals, whole grain bread,
roots and stem tubers, because they breakdown more slowly to release glucose.Avoid simple
sugars, sugar-sweetened beverages and honey.
Fats should provide < 30% ofenergy,A lower fat intake of up to 20% or less of
the daily energy in case of obese adult with diabetes.
3.Limit salt to less than 1 teaspoonful/day
4.Limit fat intake
5.Physical activity
o Aerobic (e.g. brisk walking) and muscle strengthening activities improve
glucose
tolerance, energy expenditure, feeling of wellbeing and mood, work capacity,
improved blood pressure, lipid profiles and increased functional mobility in
older people.
o Adjust medicine dosages and or food intake to avoid hypoglycaemia.
6.No smoking
7. Avoid or limit alcohol intake to one drink/day for women, two drinks/day for
men
 Pharmacological Treatment
Treatment with oral hypoglycemics
• Review the blood glucose at follow-up clinic and adjust medicines as needed until blood glucose is controlled.
• If lifestyle measures on their own failure achieve blood glucose control or blood glucose levels are persistently
high (fasting >11 mmol/l or random >15 mmol/l) initiate:
A: metformin (PO) 500mg 12hourly with or after meals. Increase, as required, until a maximum of 2000mg in 2–3
divided doses.
If Metformin is contraindicated, then use
A: glibenclamide (PO) 2.5–10mg 12hourly
OR
C: glimepiride (PO) 1–4mg 12hourly
OR
A: gliclazide (PO) 40–160mg 12hourly
If the maximum dose of metformin does not result in adequate glycaemic control, either one
of the above sulphonylureas may be added, starting with the lower dose and increasing until
control is achieved or the maximum dose is reached.
• If a combination of both medicines is still inadequate, then insulin should be added as
detailed below in the section on insulin.
NOTE:
 Activity of sulphonylureas is prolonged in both hepatic and renal failure
• Metformin is contraindicated in those with severe renal, liver and cardiac failure.
• The lower dosage is appropriate when initiating treatment in elderly patients with uncertain meal
schedules, or in patients with mild hyperglycemia
• Sulphonylureas are best taken 15 to 30 minutes before meals
Treatment with Insulin Injection in Type 2 Diabetes
Insulin injections are indicated in T2DM in the following conditions:
• Initial presentation with fasting blood glucose more than 15 mmol/l
• Presentation in hyperglycaemic emergency
• Peri-operative period especially major or emergency surgery
• Other medical conditions requiring tight glycaemic control
• Organ failure: Renal, liver, heart etc,
• Diabetes not well controlled with diet or oral drugs
• Latent autoimmune diabetes of adults (LADA)
• Contraindications to oral drugs
Types of Insulin as per WHO Essential Medicine List
TYPE OF INSULIN NAME BASAL / SHORT ACTING

SHORT ACTING A:INSULIN SHORT ACTING(Human) SHORT ACTING

SOLUBLE

INTERMEDIATE ACTING A:INSULIN INTERMEDIATE ACTING BASAL

PRE-MIXED INSULIN A:INTERMEDIATE AND SHORT BASAL + SHORT ACTING

ACTING INSULIN(70/30)

Insulin as substitution therapy

Oral medicines are discontinued (except metformin if patient is obese)
S: Pre-mixed insulin is introduced at a dosage of 0.2 IU/kg body weight and this is split into:
⅔ in the morning and ⅓ in the evening
• Inject 30 minutes before the morning and the evening meals for human insulins
• Inject 0 to 15minutes before meal for analog insulins.
PHARMACOLOGICAL TREATMENT
Total dose of insulin contains soluble and intermediate/long-acting insulin.
Give total dose of insulin
o pre puberty 0.5 IU/kg/day subcutaneously for life
o puberty 1-2 IU/kg/day subcutaneously for life
o after puberty < 2 IU/kg/day subcutaneously for life
• Divide total insulin dose as per recommended percentage below
Recommended Insulin Dosage
TIME TYPE OF INSULIN PROPORTION

Breakfast SHORT ACTING 30% of total daily dose

lunch SHORT ACTING 20% of total daily dose

Supper SHORT ACTING 10% of total daily dose

Bedtime LONG/INTERMEDIATE ACTING 40% of total daily dose

Clinical Monitoring of People with Diabetes
INITIAL VISIT
History and diagnosis
Physical examination
Height and weight,Waist/Hip circumference,Blood pressure, Detailed foot examination,Tooth inspection, Eye
examination
Visual acuity+ Fundoscopy,ECG, Biochemistry, Blood sugar, Glycosylated Haemoglobin(HbA1c), Lipid profile
(TC, HDC, LDLC,TG)
TC=Total cholesterol, HDLC=high density lipoprotein, LDLC= low density lipoprotein, G=Triglycerides
Serum creatinine,Urine: glucose, ketones, protein
• Education,Nutritional advice,Medication if needed
3MONTHS VISIT
Relevant historyWeight,Blood pressure, Foot inspection,Blood Glucose
Urine protein
• Education advice,Nutrition advice, Review therapy,HbA1c every six months
ANNUAL VISIT:History and examination – as at initial visit
Biochemistry as at initial visit
Diabetes
Mellitus

By YASIN M, MD
Introduction
• Diabetes mellitus (DM) comprises a group of common
metabolic disorders that present with hyperglycemia
(elevated blood glucose).
• Defect in body energy regulation and utilization leading to
multi-organ complications and early mortality.
Cont…
• Hyperglycemia is a cardinal manifestation due to insulin
deficiency or insulin resistance.
• Several distinct types of DM exist and are caused by a
complex interaction of genetics, environmental factors and
life-style choices.
Cont…
Depending on the etiology of DM, factors contributing to
hyperglycemia may include
• Reduced insulin secretion
• Decreased glucose usage, and
• Increased glucose production
Cont…
• The metabolic dysregulation associated with DM causes
secondary pathophysiologic changes in multiple organ
systems that impose a tremendous burden on the individual
with diabetes and on the health care system.
Classification of Diabetes
Mellitus
• Recent changes in classification reflect an effort to classify
DM on the basis of the pathogenic process that leads to
hyperglycemia, as opposed to criteria such as age of onset or
type of therapy.
• Two broad categories of DM are designated type 1(A & B)
and type 2.
Cont…
• Type 1A DM results from autoimmune beta cell destruction
which usually leads to insulin deficiency.
• Type 1B DM is also characterized by insulin deficiency as well
as a tendency to develop ketosis. The mechanisms leading to
beta cell destruction in these patients are unknown.
Cont…
• Type 2 DM is a heterogeneous group of disorders usually
characterized by variable degrees of insulin resistance,
impaired insulin secretion, and increased glucose production.
Cont…
• The terms insulin-dependent diabetes mellitus (IDDM) and
noninsulin-dependent diabetes mellitus (NIDDM) are
outdated because many individuals with type 2 DM
eventually require insulin treatment for control of glycemia,
the use of the latter term generated considerable confusion.
Risk Factors for Type 2 Diabetes
Mellitus
• Family history of diabetes (i.e. parent or sibling with type 2
diabetes)
• Obesity i.e. body mass index (BMI) >27kg/m2
• Age >45 years
• History of gestational diabetes mellitus
Cont…
• Hypertension
• Low density lipoprotein (LDL) cholesterol <0.90 mmol/l
(35mg/dl)
• In HIV patients, the HAART therapy can increase risk of
diabetes
Other Types of Diabetes Mellitus

• Other etiologies for DM include specific genetic defects in

insulin secretion or action, metabolic abnormalities that
impair insulin secretion, and a host of conditions that impair
glucose tolerance.
Cont…
Gestational Diabetes Mellitus (GDM)
• Glucose intolerance may develop and first become
recognized during pregnancy.
Clinical Features
Possible clinical features of DM depend on the severity of
disease and its complications. These are listed below;
• Polyuria
• Polydipsia
• Polyphagia
• Hyperglycaemia
Cont…
• Glycosuria
• Ketosis, Acidosis
• Coma
• Weight loss
• Fatigue
Cont….
• Weakness
• Blurred vision
• Frequent superficial infections e.g. vaginitis, fungal skin
infections
• Slow healing of skin lesions after minor trauma
Cont…
• Metabolic derangements relate mostly to hyperglycemia
(osmotic diuresis, reduced glucose entry into muscle) and to
the catabolic state of the patient (urinary loss of glucose and
calories, muscle breakdown due to protein degradation and
decreased protein synthesis).
Cont…
• Blurred vision results from changes in the water content of
the lens and resolves as the hyperglycemia is controlled.
Investigations

At primary health care facilities, the following can be done to

patients suspected of having DM.
• Fasting blood sugar
• Urine for sugar
• Random blood sugar
Cont…
• This can be done using simple devices e.g. glucometers and
urine dipsticks.
• When DM is diagnosed, patients should be referred to
hospitals for further investigations to rule out complications
and for initiation of the right medications.
Criteria for Diagnosis of
Diabetes Mellitus
• Symptoms of diabetes plus random blood glucose concentration
equal or greater than 11.1 mmol/L (200 mg/dl) or
• Fasting plasma glucose equal or greater than7.0 mmol/L (126 mg/dl)
• In the absence of unequivocal hyperglycemia and acute metabolic
decompensation, these criteria should be confirmed by repeat testing
on a different day.
Cont…
• Random is defined as without regard to time since last meal
• Fasting is defined as no caloric intake for at least 8 hours
Cont…
Glucose tolerance is classified into three categories based on the
Fasting Plasma Glucose (FPG)
• FPG < 6.1 mmol/l (110 mg/dL) is considered normal
• FPG 6.1 mmol/l (110 mg/dl) but < 7.0 mmol/l (126 mg/dl) is defined
as impaired Fasting Glucose (IFG)
• FPG 7.0 mmol/l (126 mg/dl) warrants the diagnosis of DM
Treatment
• Treatment of DM should be initiated at hospital levels after
thorough evaluation including that of the complications.
Thereafter, when patients are stable, follow up may be done
at health centres.
Cont…
Overall Principles
The goals of therapy for type 1 or type 2 DM are to;
• Eliminate symptoms related to hyperglycemia
• Reduce or eliminate the long-term microvascular and
macrovascular complications of DM
Cont…

• Allow the patient to achieve as normal a life-style as

possible
• The care of an individual with either type 1 or type 2
DM requires a multidisciplinary team
• Central to the success of this team are the patient's
participation, input and enthusiasm all of which are
essential for optimal diabetes management
Cont…
Education for Patient with Diabetes Mellitus on Nutrition and Exercise
• Patient participation is an essential component of comprehensive
diabetes care
• The patient with type 1 or type 2 DM should receive education about
nutrition, exercise, care of diabetes during illness and medications to
lower the plasma glucose.
Cont…
• Nutrition education should focus on balanced healthy eating
(avoidance of alcohol, high sugar foods such as desserts).
Cont…
• Regular daily exercise is important, recommendation is 20-30
minutes of exercise daily (this can be walking).
• Patients should also be educated as to the long term
consequences of uncontrolled diabetes (renal impairment,
higher risk of ocular damage, increased risk of heart attack,
and neuropathy).
Cont…
• Along with improved compliance patient education allows
individuals with DM to assume greater responsibility for their
care.
• Patient education should be viewed as a continuing process
with regular visits for reinforcement; it should not be a
process that is completed after one or two visits to a nurse
educator or nutritionist.
Monitoring Level of Glycemic
Control
• Optimal monitoring of glycemic control involves plasma
glucose measurements by the patient and an assessment of
long-term control by the physician measurement of
glycosylated haemoglobin (GHb ) and review of the patient's
self-measurements of plasma glucose.
Cont…
• These measurements are complementary; the patient's
measurements provide a picture of short-term glycemic
control whereas the GHb reflects average glycemic control
over the previous 2 to 3 months.
• Integration of both measurements provides an accurate
assessment of the glycemic control achieved.
Type I Diabetes Mellitus
Insulin Regimens
• In all regimens long-acting insulin (lente, ultralente, or
glargine insulin) supply basal insulin whereas prandial insulin
is provided by either regular or lispro insulin.
• Lispro should be injected just before a meal.
• Regular insulin is given 30 to 45 min prior to a meal.
Cont…
• No insulin regimen reproduces the precise insulin secretory
pattern of the pancreatic islet.
• In general individuals with type 1 DM require 0.5 to 1.0
Unit/kg per day of insulin divided into multiple doses.
Cont…
• Initial insulin-dosing regimens should be conservative
approximately 40 to 50% of the insulin should be given as
basal insulin to avoid hypoglycemia (which can be a serious
side effect of treatment of diabetes).
• A single daily injection of insulin is not appropriate therapy in
type 1 DM.
Cont…
• One commonly used regimen consists of twice-daily (2/3)
injections of an intermediate insulin (NPH or lente) mixed
with a short-acting insulin before the morning and evening
meal.
Cont…
• Such regimens usually prescribe two-thirds of the total daily
insulin dose in the morning (with about two-thirds given as
intermediate-acting insulin and one-third as short-acting)
and
• one-third before the evening meal (with approximately one-
half given as intermediate-acting insulin and one-half as
short-acting).
Type 2 Diabetes Mellitus

General Aspects
• The goals of therapy for type 2 DM are similar to those in type
1
• While glycemic control tends to dominate the management of
type 1 DM, the care of individuals with type 2 DM must also
include attention to the treatment of conditions associated
with type 2 DM (obesity, hypertension, dyslipidemia,
cardiovascular disease) and detection/management of DM-
related complications.
Cont…
• DM-specific complications may be present in up to 20 to 50%
of individuals with newly diagnosed type 2 DM.
• Reduction in cardiovascular risk is of paramount importance
as this is the leading cause of mortality in these individuals.
Cont…
Glucose Lowering Agents
Based on their mechanisms of action, oral glucose-lowering
agents are subdivided into agents that;
• Increase insulin secretion
• Reduce glucose production or
• Increase insulin sensitivity
Cont…
• Oral glucose-lowering agents (with the exception of alpha-
glucosidase inhibitors) are ineffective in type 1 DM and
should not be used for glucose management of severely ill
individuals with type 2 DM.
• Insulin is sometimes the initial glucose-lowering agent even
in type 2 DM.
Oral Glucose Lowering Agents

• Insulin secretagogues
First generation sulfonylurea
Second generation sulfonylurea
• Biguanides (metformin)- this is usually the first drug of
choice if available for type 2 diabetes as long as there are no
contraindications (e.g., in renal failure).
Cont…
• Thiazolidinediones - these are less favored for treatment
given their recent complications and side effects.
• Alpha-glucosidase inhibitors - also less effective as initial
therapy.
Complications
Cont…
• Individuals with previously undetected type 2 DM may
present with chronic complications of DM at the time of
diagnosis.
• The history and physical examination should assess for
symptoms or signs of acute hyperglycemia and should screen
for the chronic complications and conditions associated with
DM.
Acute Complications
• Diabetic ketoacidosis (DKA)
• Nonketotic hyperosmolar state (NKHS),
• Hypoglycemia are acute complications of diabetes.
Cont…
• DKA is seen primarily in individuals with type 1 DM, and
NKHS is seen in individuals with type 2 DM.
• Both disorders are associated with absolute or relative
insulin deficiency, volume depletion, and altered mental
status.
Cont…

• DKA and NKHS exist along a continuum of

hyperglycemia, with or without ketosis.
• Both disorders are associated with potentially serious
complications if not promptly diagnosed and treated.
• Diabetic ketoacidosis is a medical emergency and if
suspected needs immediate intervention and transfer
to the hospital
Chronic Complications of
Diabetes Mellitus
• DM and its complications produce a wide range of symptoms
and signs.
• Those secondary to acute hyperglycemia may occur at any
stage of the disease.
• Those related to chronic complications begin to appear
during the second decade of hyperglycemia.
Cont…
• Chronic complications of DM affect many organ systems and
are responsible for the majority of morbidity and mortality
associated with the disease.
• Chronic complications can be divided into vascular and
nonvascular complications.
Cont…
The vascular complications of DM are further subdivided into
Microvascular
• Retinopathy
• Neuropathy
• Nephropathy
Cont…
Macrovascular Complications
• Coronary Artery Disease
• Peripheral Vascular disease leading to diabetic foot
• Cerebrovascular disease
Cont…
Nonvascular complications include problems such as
• Gastroparesis
• Sexual dysfunction
• Skin changes
Cont…
• This division is rather arbitrary since it is likely that multiple
pathogenic processes are involved in all forms of
complications.
• The risk of chronic complications increases as a function of
the duration of hyperglycemia.
Cont…
• They usually become apparent in the second decade of
hyperglycemia.
• Since type 2 DM may have a long asymptomatic period of
hyperglycemia, many individuals with type 2 DM have
complications at the time of diagnosis.
THANKS FOR LISTENING
BRONCHIAL
ASTHMA

DR.MUTTA
Learning Objectives

By the end of this session, students are expected to be able to:

• Define bronchial asthma
• Classify bronchial asthma
• Mention causes of bronchial asthma
• Describe epidemiology of bronchial asthma
• Describe symptoms and signs of bronchial asthma
• Identify differential diagnoses of bronchial asthma
• Identify relevant investigations and complication for bronchial asthma
• Describe treatment of bronchial asthma
Definition of Bronchial Asthma

Asthma: A disorder characterized by chronic inflammatory reversible

airways obstruction and increased airways hyper responsiveness to
variety of stimuli that causes recurrent episodes of wheezing,
breathlessness, chest tightness and coughing.
• It is a chronic condition involving the respiratory system in which the
airways occasionally constrict, become inflamed, and are lined with
excessive amounts of mucus, often in response to one or more
triggers.
Definition of Bronchial Asthma
cont..
• Bronchial asthma may be either episodic or chronic.
• There is tendency for atopic individuals (highly sensitive pple) to
develop episodic asthma and non atopic individuals to develop
chronic asthma.
Classification of Bronchial
Asthma
Bronchial asthma may be classified into two types
 Extrinsic asthma (early onset or childhood asthma).
 Intrinsic asthma (late onset or adulthood asthma)
Cont….
Variables Extrinsic Asthma Intrinsic Asthma

Prevalence 10-12% < 2%

Cause Hereditary Acquired

Persons Affected *Atopic individuals *Non-Atopic Individuals

Type of Asthma Episodic asthma Chronic Asthma

Onset Childhood Adulthood

Triggering Factors Apparent Not Clear

Allergic Skin Test Positive Negative

Allergic Disorders e.g. Eczema, Atopic Present Absent

Dermatitis, Allergic Rhinitis, Urticaria
Family History of Allergic Disorders Present Absent
Including Extrinsic Asthma
Seasonal Fluctuations Worse in Summer Worse in Winter
Classification
Atopic individuals are people having familial hereditary tendency of
asthma or other allergic disorders while
Non-atopic individuals are the ones who become asthmatic after
exposure to high doses of allergens e.g. at work as in carpenters
(sawdust) and farmers (pollens).
CONT…
Episodic Asthma
• In episodic asthma the patient has no respiratory symptoms between
episodes, or signs of asthma.
• Paroxysm of wheeze and dyspnoea may occur at any time and can be
of sudden onset.
Cont….
Chronic Asthma
• Symptoms of chest tightness wheeze and breathlessness on exertion
together with spontaneous cough and wheeze during the night and
early in the morning may be chronic unless controlled by appropriate
drugs.
• Severe asthma persisting from childhood may form a pigeon chest
deformity.
Epidemiology of Bronchial Asthma

Race
• According to cause Bronchial asthma occurs in persons of all races worldwide.

Sex
• Bronchial asthma predominantly occurs in boys in childhood with a male to female ratio
of 2:1 till puberty.
• Asthma prevalence is greater in females after puberty and majority of adult onset cases
diagnosed in persons older than 40 years occurs in females.
• Boys are more likely than girls to experience decrease in symptoms by late adolescence.
Epidemiology of Bronchial Asthma
cont..
Age
• Bronchial asthma prevalence is high in very young persons and very old persons
because of airways hyper responsiveness and lower levels of lung function

Occupation
High risk jobs are
• Farming
• Painting
• Janitorial work
• Plastic manufacturing
Aetiology

• Asthma is caused by a complex interaction of environmental and

genetic factors that researchers do not yet fully understand.
• These factors can also influence how severe a person’s asthma is
and how well they respond to medication.
• Environmental tobacco smoke, especially maternal cigarette
smoking, is associated with high risk of asthma prevalence and
asthma morbidity, wheeze, and respiratory infections.
• Poor air quality, from traffic pollution or high ozone levels, has
been repeatedly associated with increased asthma morbidity
Aetiology cont..

Genetic
• Over 100 genes have been associated with asthma in at least one
genetic association study.
• Gene-environment Interactions
• Research suggests that some genetic variants may only cause asthma
when they are combined with specific environmental exposures, and
otherwise may not be risk factors for asthma.
Pathology

• Airways obstruction is caused by Bronchoconstriction

• During an asthma episode, inflamed airways react to environmental triggers
such as smoke, dust, or pollen.
• The airways narrow and produce excess mucus, making it difficult to breathe.
Pathology cont..
• In essence, asthma is the result of an immune response in the bronchial
airways.
• The airways of asthmatics are "hypersensitive" to certain triggers, also known
as stimuli. In response to exposure to these triggers, the bronchi (large
airways) contract into spasm (an asthma attack).
• Inflammation soon follows, leading to a further narrowing of the airways and
excessive mucus production, which leads to coughing and other breathing
difficulties.
Pathology cont..
• Airways oedema
• Chronic mucous plug formation. It consists of an exudate of serum proteins
and cell debris that may take weeks to resolve.
• Airways remodeling: It is associated with structural changes due to long
standing inflammation and may profoundly affect the extent of reversibility of
the airways obstruction.
Atopy
The triad of:
• Asthma
• Eczema
• Allergic Rhinitis

These 3 conditions are often inherited together an may be present

together in a single patient or family.
Figure showing Pathological Changes in Bronchial Asthma
Symptoms of Asthma

• Productive cough
• Wheezing
• Shortness of breath
• Chest tightness
• Decrease exercise tolerance
• Symptoms such as cough and wheeze are commonly occurring at
night and disturb sleep
Signs of Asthma

• General evidence of respiratory distress

• Increased respiratory rate
• Increased heart rate
• Diaphoresis( persipiration/sweating)
• Use of accessory muscles of respiration
• Marked weight loss may indicate severe emphysema
Chest Examination

• Barrel chest
• End-respiratory rhonchi or prolonged expiratory phase
• Diminished breath sounds and chest hyperinflation may be observed
during acute exacerbations
• Severe asthma persisting from childhood may cause a ‘pigeon chest’
deformity (pectus carinatum)
Features of Acute Severe Asthma in Adult

• Patient cannot complete a sentence

• Pulse rate >110bpm
• Respiratory rate >25bpm
Features of Life Threatening Asthma in
Adult
• Silent chest
• Cannot speak
• Confusion or reduced level of consciousness
• Cyanosis
• Bradycardia or arrhythmias
• Hypotension
• Exhaustion
• Confusion
• Coma
• Near fatal asthma: Patients have raised PaCO2
Complications of Asthma

• Pneumonia
• Pneumothorax
• Respiratory failure
• Complications from corticosteroids
• Osteoporosis ( fragile bones especial in women)
• Immunosuppression
• Cataract
• Myopathy
• Weight gain
• Addisonian crisis
• Thinning of the skin
•
Diagnosis of Asthma
The diagnosis of asthma is made by history, physical and CXR but can be
confirmed by spirometry (if available) or peak flow meter
• On spirometry: FEV1/FVC ratio that improves with beta-agonist
• On peak flow meter: reduced peak flow (for height and age)
Differential Diagnosis
1. Bacterial pneumonia (if fever) - may be the trigger for asthma
2. PCP (if HIV positive)
3. Pulmonary edema (if CCF)
4. COPD-emphysema and bronchitis (if smoker)
5. PE (if DVT)
6. TB (if chronic and fever, NS or wt loss)
7. Helminth infection (migration of larvae)
8. Foreign body aspiration
9. Congenital airway obstruction (children)
“Not all that wheezes is asthma”
Investigations

• Full Blood Picture

• Eosinophilia of greater than 4% or 300-400 cells/ml supports the diagnosis of asthma
• Radiography
• Normal
• Show signs of hyperinflation, indistinguishable from that of emphysema
• Show ‘pigeon chest’ deformity in the lateral view
• Show opacity caused by lobar or segmental collapse when a large bronchus is
obstructed by tenacious mucus
• Sputum
• Gram stain
• Ziehl-nelsen stain
Treatment of Asthma Attack
• Based on Severity of Attack
• All patients with severe or life-threatening asthma should be admitted to the
hospital.
• In severe asthma patients will be unable to speak in full sentences, RR>25,
HR>105.
• In life-threatening asthma patients will have silent chest, cyanosis,
bradycardia, hypotension, feeble respiratory effort or confusions and these
patients should be admitted to the ICU.
• Status asthmaticus is life-threatening asthma that does not improve with
treatment
(Source: Oxford Handbook)
Treatment

• Acute severe asthma and life threatening asthma in adult

Perform pre-referral treatment :
give
• Nebulized sulbutamol or inhaled salbutamol (if available)
• Hydrocortisone 200mg i.v slowly (if available)
• Aminophylline 250mg i.v slowly or tabs
• Monitor vital signs
• Refer to higher centre immediately
Treatment (at Higher Centre)

• Oxygen 40-60% via nasal prongs or face mask if available

• Nebulized sulbutamol or inhaled salbutamol delivered by a spacer
• Hydrocortisone 200mg i.v slowly then oral prednisolone 30-60mg for
5-7 days
• Aminophylline 250mg i.v slowly or tabs when therapy above fails
Use of Inhaler
Counseling on Use of Inhaler
1) Expire forcefully and completely
2) Hold breath and place inhaler on lips
3) Push the button and breath in slowly to maximal inspiration
 Use of Spacer

* spacers are better than inhaler alone in children and adults with severe symptoms. Can be
made from Dasani water bottle.
Goals of Therapy in the Treatment of Chronic Asthma

• Achieve and maintain control of symptoms

• Prevent asthma exacerbations
• Maintain pulmonary functions as close to normal levels as possible
• Maintain normal activity levels, including exercise
• Avoid adverse effects from asthma medications
• Prevent the development of irreversible airflow limitation
• Prevent asthma mortality
Management of Chronic Persistent Asthma

Step-I:
• Occasional Use of Inhaled Short-Acting Beta2-Receptor Agonist
• Indications
• Intermittent symptoms occurring less than once a week
• No daily medication needed
• Treatment
• Long term control (controller medication): Not required
• Quick relief (reliever medication) : A short-acting beta2-receptor agonist inhaler
• Dose
• Metered doses inhaler (MDI): 1-2 puff when required (PRN)
• Nebulizer: Dilute 0.5 ml (2.5 mg) of 0.5% inhalation solution in 1-2.5 mls of normal saline or water for
injection, administer 2.5-5 mg when required (PRN).
Management of Chronic
Persistent Asthma cont..
Step-II:
• Regular Use of Inhaled Anti-Inflammatory Agents
• Indications
• Symptoms occurring more than once a week but less than once a day
• Patient using beta2-adrenoceptor agonist more than once daily
• Treatment
• Reliever medication (bronchodilator): A short-acting beta2-adrenoreceptor agonist inhaler
• Metered doses inhaler (MDI): 1-2 puff every 4-6 hrs, not to exceed 12 puffs/day
• Nebulizer: Dilute 0.5 mL (2.5 mg) 0.5% inhalation solution in 1-2.5 mls of normal saline or
water for injection; administer 2.5-5 mg every 4-6 hrs. Plus
• Controller medication: (anti-inflammatory)
• Inhaled corticosteroids: Beclometasone (up to 800 ug daily)
Management of Chronic
Persistent Asthma cont..
Step-III:
• High Dose Inhaled Corticosteroids or Low Dose Inhaled Corticosteroids Plus a Long-Acting Inhaled
Beta2-Adrenoceptor Agonist
• Indication: Daily symptoms
• Treatment
• Reliever medication: A short-acting beta2-adrenoreceptor agonist inhaler given as
required (PRN)
• Controller medication: Inhaled corticosteroids e.g. Beclometasone, Plus
• Long-acting bronchodilator such as beta2-adrenoreceptor agonist e.g. Formoterol
fumarate 6 ug 12 hourly or Salmeterol 50 ug 12 hourly or aminophylline may be
added
• In patients whose asthma is poorly controlled by inhaled corticosteroids, the
addition of a long-acting beta2-receptor agonist improves symptoms and lung
function and reduces exacerbations
Step-IV:
• High Dose Inhaled Corticosteroids and Regular Bronchodilators
• Indications: Failure of step-III medications
• Treatment
• Reliever medication: A short-acting beta2-adrenoreceptor agonist inhaler
given as required (PRN)
• Controller medication: Inhaled corticosteroids e.g. Beclometasone in a dose
range 800-2000 ug daily, plus.
Step-V:
• Addition of Regular Oral Corticosteroid Therapy
• Indications: Failure of step-IV medications
• Treatment
• Step-IV medications. Plus
• Regular Prednisolone tablets prescribed in the lowest amount necessary to
control symptoms as a single daily dose in the mornings
Step V cont..
Patient’s Education
• It should begins at the time of diagnosis and be revisited in every
subsequent consultation.
• Education involves the patient understanding the nature of asthma, the
practical skills necessary to manage asthma successfully e.g. using inhaler
devices and monitor the effect of treatment and the severity of
exacerbations with spirometer and the adoption of appropriate actions in
responses to deteriorating asthma.
• Patients should appreciate the differences between the reliever medication
(bronchodilator) and the controller medication (anti-inflammatory).
Stage V cont..
Antibiotics
• They should be reserved for patients with fever and purulent sputum or other evidence of pneumonia
or sinusitis.

Hydration
• Aggressive hydration is not recommended for adults,
• Chest physiotherapy, mucolytics and sedation are not recommended.
Diet
• No special diet is generally indicated.

Activities
• No specific limitations are recommended for patients with asthma.
• Prevention of Asthmatic Attack
• Avoidance of exposure to allergen to which patients are sensitive to:
• Animal dander: Avoid contact with dogs, cats, horses or other animals.
• Feathers in pillows or quilts: Substitute latex foam pillows and terylene quilts.
• Avoid all preparations of relevant drugs e.g.beta-blockers, aspirin and other
non-steroidal anti-inflammatory drugs if the patient is sensitive.
• Prevention of Asthmatic Attack cont..
• Food: Identify and eliminate from diet.
• Industrial chemicals e.g. isocyanates, epoxy resins, perfumes: Avoid exposure
to chemical or change occupation.
• Do not smoke and avoid environmental smoke.
• Pollens: Try to avoid exposure to flowering vegetation and keep the bedroom
windows closed.
• Avoid exertion during high levels of pollution.
Prevention of Asthmatic Attack cont..
Exercise Induced Asthma
• A warm-up period of 15 minutes is recommended prior to the scheduled exercise
event. This approach is not helpful for unscheduled events, prolonged exercise or
elite athletes
• Use of Inhaled medications

Drug Used
• Inhaled short acting beta2 agonist: e.g. Salbutamol given 15-30 prior to exercise.
• Inhaled mast cell stabilizers: e.g. sodium cromolyn given 15-30 prior to exercise.
Prevention of Asthmatic Attack cont..
Others
• Long acting beta2agonist (given 90 minutes prior to exercise) for
repetitive exercise
• Leukotriene antagonist
• Inhaled heparin
• Inhaled Frusemide
Prognosis
• The prognosis of individual asthma attacks is generally good.
• Seasonal fluctuations can occur in both types of asthma, atopic
subjects with episodic asthma are usually worse in the summer when
they are more heavily exposed to antigens while chronic asthmatic
patients are usually worse in winter months because of the increased
frequency of viral infections.
Key Points

• Bronchial asthmatic episodes are aggravated by either intrinsic or

extrinsic factors.
• Educating patients with bronchial asthma should start early when
diagnosis is established in order to carry out necessary precautions.
• Severe bronchial asthma is an emergency which need urgent
attention.
Evaluation

• List clinical features of asthma.

• What are the differential diagnoses of Bronchial Asthma?
• What is the treatment of severe Bronchial asthma?
Bronchi
al
Asthma

By YASIN
M, MD
Introduction
Asthma is a disorder characterized by chronic inflammatory
reversible airways obstruction and increased airways
hyperresponsiveness to variety of stimuli that causes
recurrent episodes of wheezing, breathlessness, chest
tightness and coughing.
Cont…
It is a chronic condition involving the respiratory system in
which the airways occasionally constrict, become inflamed,
and are lined with excessive amounts of mucus, often in
response to one or more triggers.
Bronchial asthma may be either episodic or chronic.
There is tendency for atopic individuals to develop episodic
asthma and non atopic individuals to develop chronic asthma.
Classification
Bronchial asthma may be classified into two types
Extrinsic asthma (early onset or childhood asthma).
Intrinsic asthma (late onset or adulthood asthma)
DIFFERENCES BETWEEN
INTRINSIC AND EXTRINSIC
ASTHMA
Variables Extrinsic Asthma Intrinsic Asthma
Prevalence 10-12% < 2%
Cause Hereditary Acquired
Persons Affected Atopic individuals Non-Atopic
Type of Asthma Episodic asthma Chronic Asthma
Onset Childhood Adulthood
Triggering Factors Apparent Not Clear
Allergic Skin Test Positive Negative
Allergic Disorders e.g. Present Absent
Eczema, Atopic Dermatitis,
Allergic Rhinitis, Urticaria
Family History of Allergic Present Absent
Disorders Including Extrinsic
Asthma
Seasonal Fluctuations Worse in Summer Worse in Winter
Cont…
Episodic Asthma
• In episodic asthma the patient has no respiratory symptoms
between episodes, or signs of asthma.
• Paroxysm of wheeze and dyspnoea may occur at any time
and can be of sudden onset.
 Cont…
Chronic Asthma
• Symptoms of chest tightness wheeze and
breathlessness on exertion together with
spontaneous cough and wheeze during the
night and early in the morning may be chronic
unless controlled by appropriate drugs.
• Severe asthma persisting from childhood may
form a pigeon chest deformity
Aetiology & Epidemiology of
Bronchial Asthma
Race
• According to cause Bronchial asthma occurs in persons of all
races worldwide
Sex
• Bronchial asthma predominantly occurs in boys in childhood
with a male to female ratio of 2:1 till puberty.
Cont…
• Asthma prevalence is greater in females after puberty and
majority of adult onset cases diagnosed in persons older
than 40 years occurs in females.
• Boys are more likely than girls to experience decrease in
symptoms by late adolescence.
Cont…
Age
• Bronchial asthma prevalence is high in very young persons
and very old persons because of airways
hyperresponsiveness and lower levels of lung function
Cont…

Occupation
High risk jobs are
• Farming
• Painting
• Janitorial work
• Plastic manufacturing
Causes
• Asthma is caused by a complex interaction of environmental
and genetic factors that researchers do not yet fully
understand.
• These factors can also influence how severe a person’s
asthma is and how well they respond to medication.
Cont…
• Environmental tobacco smoke, especially maternal cigarette
smoking, is associated with high risk of asthma prevalence
and asthma morbidity, wheeze, and respiratory infections.
• Poor air quality, from traffic pollution or high ozone levels,
has been repeatedly associated with increased asthma
morbidity
Cont…
Genetic
• Over 100 genes have been associated with asthma in at least one
genetic association study.
Gene-environment Interactions
• Research suggests that some genetic variants may only cause asthma
when they are combined with specific environmental exposures, and
otherwise may not be risk factors for asthma.
Precipitating or
Aggravating
Factors
Factors Contributes to Bronchial Asthma
or Airways Hyper Responsiveness
Environmental allergens
• House dust mites
• Wood dusts
• Cockroach allergens
• Fungal spores
• Plants
• Animal allergens especially from cats and dogs
• Feathers in pillow and mattresses
Cont…
Food e.g. fish, eggs, milk, yeast, and wheat which reaches the
bronchi via blood stream
Environmental pollutants e.g. smoke from tobacco, industries, cars,
firewood
Irritants e.g. house hold sprays, paints and perfumes
Cont…

Industrial chemicals
• Isocyanates
• Anhydrides
• Epoxy resin
Drugs
• Aspirin or NSAIDS
• Non-selective beta-blockers including ophthalmic preparations
e.g. Propranolol
Cont…
Exercise or hyperventilation
Emotion
Stress e.g. infections or trauma
Gastroesophageal reflux disease (GERD)
Infection: Viral or bacterial infections of the respiratory system
Factors Contributes to Exercise-Induced Asthma

• Exposure to cold or dry air

• Environmental pollutants e.g. sulphur, ozone
• Levels of bronchial hyperactivity
• Chronicity of asthma and symptomatic control
Cont…
• Duration and intensity of exercise
• Allergen exposure in Atopic individuals
• Co-existing respiratory infection
Pathology

Airways obstruction is caused by

Bronchoconstriction
• During an asthma episode, inflamed airways react to
environmental triggers such as smoke, dust, or pollen.
• The airways narrow and produce excess mucus, making it
difficult to breathe.
• In essence, asthma is the result of an immune response in
the bronchial airways.
Cont…
• The airways of asthmatics are "hypersensitive" to certain triggers, also
known as stimuli. In response to exposure to these triggers, the
bronchi (large airways) contract into spasm (an "asthma attack").
• Inflammation soon follows, leading to a further narrowing of the
airways and excessive mucus production, which leads to coughing and
other breathing difficulties
Cont…
Airways oedema
Chronic mucous plug formation. It consists of an exudate of serum
proteins and cell debris that may take weeks to resolve.
Airways remodeling: It is associated with structural changes due to
long standing inflammation and may profoundly affect the extent of
reversibility of the airways obstruction.
Symptoms of Asthma

• Productive cough
• Wheezing
• Shortness of breath
• Chest tightness
• Decrease exercise tolerance
• Symptoms such as cough and wheeze are commonly occurring at
night and disturb sleep
Signs of Asthma
• General evidence of respiratory distress
• Increased respiratory rate
• Increased heart rate
• Diaphoresis
• Use of accessory muscles of respiration
• Marked weight loss may indicate severe emphysema
Chest Examination

• Barrel chest
• End-respiratory rhonchi or prolonged expiratory phase
• Diminished breath sounds and chest hyperinflation may be observed
during acute exacerbations
• Severe asthma persisting from childhood may cause a ‘pigeon chest’
deformity (pectus carinatum)
Features of Acute Severe
Asthma in Adult
• Patient cannot complete a sentence
• Pulse rate >110bpm
• Respiratory rate >25bpm
Features of Life Threatening Asthma in Adult

• Silent chest
• Cannot speak
• Confusion or reduced level of consciousness
• Cyanosis
• Bradycardia or arrhythmias
Cont…
• Hypotension
• Exhaustion
• Confusion
• Coma
• Near fatal asthma: Patients have raised PaCO2
Complications of Asthma

• Pneumonia
• Pneumothorax
• Respiratory failure
Complications from corticosteroids

• Osteoporosis
• Immunosuppression
• Cataract
• Myopathy
• Weight gain
• Addisonian crisis
• Thinning of the skin
Differential Diagnosis of Asthma
• Bronchiectasis
• Pulmonary oedema
• Emphysema
Cont…
• Congestive Cardiac Failure
• Allergic rhinitis
• Pneumonia
• Tuberculosis
Investigations

• Full Blood Picture

• Eosinophilia of greater than 4% or 300-400 cells/ml supports the
diagnosis of asthma
• Radiography
• Normal
• Show signs of hyperinflation, indistinguishable from that of
emphysema
• Show ‘pigeon chest’ deformity in the lateral view
• Show opacity caused by lobar or segmental collapse when a large
bronchus is obstructed by tenacious mucus
Cont…
• Sputum
• Gram stain
• Ziehl-nelsen stain
Note: In this case only sputum examination may be examined in the
dispensary or health centre. For the rest of the investigations, patients
need to be referred to hospital.
Treatment

Acute severe asthma and life threatening asthma in adult

• Perform pre-referral treatment : give
• Nebulized salbutamol or inhaled salbutamol (if available)
• Hydrocortisone 200mg i.v slowly (if available)
• Aminophylline 250mg i.v slowly or tabs
• Monitor vital signs
• Refer to higher center immediately
Treatment (at Higher Centre)

• Oxygen 40-60% via nasal prongs or face mask if

available
• Nebulized sulbutamol or inhaled salbutamol delivered
by a spacer
• Hydrocortisone 200mg i.v slowly then oral
prednisolone 30-60mg for 5-7 days
• Aminophylline 250mg i.v slowly or tabs when therapy
above fails
Goals of Therapy in Treatment of Chronic Asthma

• Achieve and maintain control of symptoms

• Prevent asthma exacerbations
• Maintain pulmonary functions as close to normal levels as
possible
• Maintain normal activity levels, including exercise
Cont…
• Avoid adverse effects from asthma medications
• Prevent the development of irreversible airflow limitation
• Prevent asthma mortality
Patient’s Education

• It should begins at the time of diagnosis and be revisited in every

subsequent consultation.
• Education involves the patient understanding the nature of asthma,
the practical skills necessary to manage asthma successfully e.g. using
inhaler devices and monitor the effect of treatment and the severity
of exacerbations with spirometer and the adoption of appropriate
actions in responses to deteriorating asthma.
• Patients should appreciate the differences between the reliever
medication (bronchodilator) and the controller medication (anti-
inflammatory).
Prevention of Asthmatic Attack

• Avoidance of exposure to allergen to which patients are sensitive to:

• Animal dander: Avoid contact with dogs, cats, horses or other
animals.
• Feathers in pillows or quilts: Substitute latex foam pillows and
terylene quilts.
• Avoid all preparations of relevant drugs e.g.beta-blockers, aspirin and
other nonsteroidal anti-inflammatory drugs if the patient is sensitive.
Cont…
• Food: Identify and eliminate from diet.
• Industrial chemicals e.g. isocyanates, epoxy resins, perfumes: Avoid
exposure to chemical or change occupation.
• Do not smoke and avoid environmental smoke.
• Pollens: Try to avoid exposure to flowering vegetation and keep the
bedroom windows closed.
• Avoid exertion during high levels of pollution.
Exercise Induced Asthma

• A warm-up period of 15 minutes is recommended prior to the

scheduled exercise event.
• This approach is not helpful for unscheduled events, prolonged
exercise or elite athletes
• Use of Inhaled medications
Cont…
Drug Used
• Inhaled short acting beta2 agonist: e.g. Salbutamol given 15-
30 prior to exercise.
• Inhaled mast cell stabilizers: e.g. sodium cromolyn given 15-
30 prior to exercise
Cont…
Others
• Long acting beta2agonist (given 90 minutes prior to exercise) for
repetitive exercise
• Leukotriene antagonist
• Inhaled heparin
• Inhaled Frusemide
Prognosis

• The prognosis of individual asthma attacks is generally good.

• Seasonal fluctuations can occur in both types of asthma, atopic
subjects with episodic asthma are usually worse in the summer when
they are more heavily exposed to antigens while chronic asthmatic
patients are usually worse in winter months because of the increased
frequency of viral infections.
THANKS FOR LISTENING
Asthma
STANDARD TREATMENT GUIDELINES
ASTHMA
It is a chronic reversible obstructive inflammatory airways disease in which many cells and cellular
element play a role by constriction of bronchial smooth muscle causing bronchospasm, oedema of
bronchial mucous membrane and blockage of the smaller bronchi with plug of mucous.
Clinical presentation
• wheeze,shortness of breath,chest tightness,cough This presentation particularly
at night or in the early morning,Tachypnea
• Tachycardia,
• Diffuse musical wheezes,
• Prolonged phase of exhalation,
• Chest hyperinflation.
• Use of Accessory muscle
Investigations: FBP (Look for eosinophilia), Serum IgEa,ESR,ABG,CXR if highly suspicion of
Pneumonia,Sputum for cytology a (look foreosinophilia),Lung function Test (e.g.: spirometrywith
reversibility test, PEFR measurement with a peak flow meter), Exhaled NO should be done to asses
evidence of variable expiratory airflow limitation
Non-pharmacological Treatment
• Avoid polluted environment (both indoors and outdoors)
• Avoid non-selective β-blockers,which can trigger asthmatic attack
• Avoid heavy exercise
Note:The management of asthma in children is like that in adult. Infants under
18 months, may not respond well in bronchodilator
• Uncertain in diagnosis should prompt early referral, because asthma-COPD
overlap has worse outcome.
• Patient intolerant of NSAIDs or who exhibit any of the high-risk clinical
features for intolerance to these drugs (severe asthma, nasal polyps or chronic
rhino sinusitis) should use NSAIDs only under close medical supervision.
Note
Patients who get night attacks should be advised to take their medication on
going to bed
 MILD MODERATE ATTACK TREATMENT
Able to talk in sentences or phrases, not agitated, pulse rate 100-120bpm
Sat 02(on air)-90-95%,PEF>50% predicted
I. Salbutamol inhalation:Give: 4-10 puffs by pMDI/ spacer/ every 20minutes for 1st hour
A: salbutamol(nebulization) Adult: Salbutamol respules 5mg 6hrly (2-3cycles and
reassess); Pediatric: 2.5mg 6hrly (2-3cycles and reassess).
If symptoms completely subside observe for 1–4hours, give Salbutamol for 24–48hours (2-
4 puffs every 4–6hours) for 3 days. If attack is only partially resolved give 2–4 puffs of
Salbutamol every 3–4 hours if attack
is mild; 6 puffs every 1–2 hours if the attack is moderate, until symptoms subside. When
attack completely resolved proceed as above.
II. prednisolone (PO): Adult 40mg am 7/7; Pediatrics 1-2mg/kg max 40mg,Do tapering if
exceed seven days.
III: Controlled oxygen (if available): target saturation 93-95% (children: 94-98%)
Note: If symptoms worsen or do not improve, treat as SEVERE ATTACK
 SEVERE ATTACK TREATMENT
• Talks in words i.e. cannot complete a Sentence in 1 breath or too breathless to talk
/feed,Sits hunched forwards, Agitated, Respiratory rate>30/min,Accessory Muscles being
Used,Pulse Rate >120 bpmO2 saturation (on air): < 90%,PEF ≤ 50% predicted or best
I. Admit the patient, place in semi-sitting position
II. Oxygen continuously 5L/min (maintain O2 saturation for adult 93-95% (children 94-98%)
III. InhalationA: salbutamol (nebulization) 4-10puffs every 20-30min in children <5years, up to
20 puffs in children >5years and adults Add S: ipratropium bromide (inhalation)0.25-0.5mg 6-
8hourly
AND
A: hydrocortisone (IV) 5mg/kg in children, 100mg in adults 6hourly then switch to oral
A: prednisolone (PO)1-2mg/kg 24hourly to complete 7days of treatment
If attack is completely resolved continue with salbutamol inhalation 2–4puffs every 4hours for
24-48hours and oral prednisolone 1-2mg/kg 24hourly to complete 3–5days of treatment.
If not improving or condition worsens, treat as LIFE-THREATENING
ATTACK
 LIFE THREATENING ATTACK
TREATMENT
• Altered level of consciousness (drowsiness, confusion, coma),Exhaustion,Silent chest,Paradoxical
thoracoabdominal movement
• Cyanosis,Collapse,Bradycardia in children or arrhythmia/ hypotension in adults
• O2 saturation<92%
TREATMENT
I. Admit the patient, place in semi-sitting position
II. Oxygen continuously 5L/min (maintain O2 saturation between 94-98%)
III. A: salbutamol (nebulization) 2.5mg for children <5years and in children >5years & adults 2.5-5mg every
20–30min then switches to salbutamol aerosol when clinical improvement is achieved.Add: S: ipratropium
bromide (inhalation) 0.25-0.5mg 6-8hourly.
AND
A: hydrocortisone (IV) 5mg/kg in children, 100mg (IV) in adults every 6hours then switch to
A: prednisolone (PO) 1-2mg/kg 24hourly to complete 7days of treatment
In adult administer a single dose of
A: magnesium sulphate (Infusion of 1-2g in 0.9% Sodium Chloride over 20 minutes)
CHRONIC ASTHMA IN ADULTS
The assessment of the frequency of daytime and nighttime symptoms and limitation of physical activity
determines whether asthma is intermittent or persistent.Therapy is stepwise (Step 1–4) based on the
category of asthma and consists of: Preventing the inflammation leading to bronchospasm (controllers)
and Relieving bronchospasm (relievers)
Controller medicines in asthma
• Inhaled corticosteroids (ICS) e.g. Beclomethasone, Budesonide, Fluticasone
• Leukotriene modifiers: e.g. Montelukast can added from step 2 patient (should be administer when low
ICS or ICS-LABA has failed to achieve desired outcome.
• long acting muscarinic antagonist (LAMA) e.g tiotropium
• Long acting β2 agonists (LABA) e.g. formoterol, salmeterol
Reliever medicines in asthma
• Short acting β2 agonists (SABA) e.g. Salbutamol
• short acting muscarinic antagonist (SAMA) e.g. ipratropium bromide (should be used in
acute asthma attack)
 Status
Asthmaticus

By
YASIN M, MD
Introduction

Status asthmaticus is an acute exacerbation

of asthma that remains unresponsive to initial
treatment with bronchodilators
OR
Status asthmaticus is a medical emergency in
which asthma symptoms are refractory to initial
bronchodilator therapy.
Patients report

• Chest tightness
• Rapidly progressive shortness of breath
• Dry cough
• Wheezing
Cont…

Typically patients present a few days after;

• The onset of a viral respiratory illness
• Following exposure to a potent allergen or irritant or
• Exercise in a cold environment
• Frequently patients have underused or have been
under prescribed anti-inflammatory therapy.
Causes of Status Asthmaticus

In persons with acute asthma, bronchospasms occur as a result

of one or more inciting factors that may include;
• A viral upper or lower respiratory tract infection
• Significant allergic response to an allergen such as
Pollen
Mold
Animal dang
House dust mites
Cont…
• Exposure to an irritant or
• Vigorous exercise in a cold environment
• Infection
• Poor adherence to the medical regimen
• Rapid decrease in long-term oral steroid therapy
Cont…
• Inflammation can be the result of
Infection
Lymphocyte, mast cell, eosinophilic, and neutrophilic
responses
Airway epithelial damage
Clinical Features of Status Asthmaticus

History
• Patients with status asthmaticus have severe dyspnea that
has developed over hours to days
• Patients usually present with audible wheezing
Physical Findings

• Patients are usually upon examination and, in early

stages of status asthmaticus, may have significant
wheezing.
• Initially wheezing is heard only during expiration but
later wheezing occurs during both expiration and
inspiration.
• The chest is hyper expanded and accessory muscles
particularly the sternocleidomastoid, scalene, and
intercostal muscles are used.
Cont…
• Later as bronchoconstriction worsens patients' wheezing
may disappear which may indicate severe airflow
obstruction.
• Normally the pulsus paradoxus (i.e. the difference in systolic
blood pressure between inspiration and expiration) does not
exceed 15 mm Hg.
Cont…
• In patients with severe asthma a pulsus paradoxus of greater
than 25 mm Hg usually indicates severe airway obstruction.
• Status asthmaticus is a medical emergency, if not managed
initially can lead to the need for intubation and ventilation.
Differential Diagnoses
• Pulmonary hypertension
• Congestive heart failure
• Upper airway obstruction
• Pneumonia (bacterial or viral)
• Chronic Obstructive Pulmonary Disease (COPD) exacerbation
• Pneumothorax
Investigations

Note: Investigations are available in equipped hospitals and therefore

patients may be referred after receiving pre-referral management. In
hospitals, the investigations that can be done are outlined below;
• Pulse oximetry values should be used to monitor the progression of
asthma
• Obtain a complete blood count (CBC) and differential count
Cont…

• Obtain an arterial blood gas

• Obtain a chest radiograph to evaluate for:
Pneumonia
Pneumothorax
Congestive heart failure
Signs of chronic obstructive pulmonary disease
These conditions may complicate patient's response to
treatment
Treatment of Status
Asthmaticus
• Patients with status asthmaticus need close monitoring as
well as oxygen therapy and therefore referring them to
hospitals with equipments is important.
• After confirming the diagnosis and assessing the severity of
the asthma attack, direct treatment is toward controlling
bronchoconstriction and further inflammation.
Cont…

Bronchodilator Treatment with Beta-2 Agonists

• The first line of therapy is bronchodilator treatment
with a beta-2 agonist is albuterol (Salbutamol).
• Handheld nebulizer treatments may be administered
either continuously (10-15 mg/h) or by frequent timing
(e.g. q5-20min), depending on the severity of the
bronchospasm.
Cont…
Oxygen therapy
Glucocorticosteroids
Steroids are the most important treatment for status asthmaticus
Fluid replacement
Intravenous fluids are administered to restore blood volume, however should
make sure the patients are not in congestive heart failure
Cont…
Antibiotics
• The routine administration of antibiotics is discouraged
• Patients are administered antibiotics only when they show
evidence of infection such as pneumonia, sinusitis
Cont…

Aminophylline (theophylline)
• Starting intravenous aminophylline may be reasonable in
patients who do not respond to medical treatment with
bronchodilators, oxygen, corticosteroids, and intravenous fluids
within 24 hours
• The loading dose is usually 5-6 mg/kg followed by a continuous
infusion of 0.5-0.9 mg/kg/h
• Aminophylline has some significant side effects and need to
monitor for therapeutic range
Complications

• Pneumothorax may complicate acute asthma either because of

increased airway pressure or as a result of mechanical ventilation.
• Superimposed infection can also occur in intubated patients.
• Patients may require a chest tube for pneumothorax or aggressive
antibiotic therapy for a superimposed infection.
THANKS FOR LISTENING
COPD
INTERNAL MEDICINE
Anatomy - Medium
Airways
Anatomy - Small Airways
COPD - Definition
• Chronic Obstructive Pulmonary Disease (COPD) is actually group of
diseases characterized by chronic, progressive, predominantly
irreversible obstructive lung disease
COPD - Epidemiology
• Extremely common worldwide affecting >10% of adults >65
years old.
• In the US and Europe, COPD is almost entirely a disease of
smokers, ex-smokers and people exposed to smokers.
• In developing countries, exposure to smoky fires in poorly
ventilated housing is another major risk factor for COPD
(elderly women)
• Other rare causes include:
• rare genetic conditions (alpha-1-antitrypsin deficiency)
• The extremely elderly
Types of COPD
1. Emphysema
2. Chronic Bronchitis
3. Chronic, poorly-treated Asthma
4. Bronchiectasis
Emphysema vs Chronic Bronchitis
• We are moving away from these terms because most patients with
COPD have both and the treatment is the same but…
• Chronic Bronchitis - productive cough for at least 3 consecutive months in at
least 2 consecutive years, usually worse in the morning; primarily a disease of
increased mucus; aka smokers cough; “blue bloaters”
• Emphysema - “pink puffers”
Clinical feature of COPD
• Chronic Bronchitis (blue bloaters)
 pt may be obese
Use of accessory muscles of respiration is common
Coarse rhonchi and wheezing heard on auscultation
Pt may have sign of right HF (Co pulmonale)
Frequent cough
Cont…
• Emphysema (pink puffers)
Patient may be very thin with barrel chest
They typically have little or no cough or expectoration
Hyperresonant and wheezing may be heard
Breathing may be assisted by use of accessory respiratory muscles.
Pathophysiology of Emphysema and
COPD
• Smoke elicits inflammatory response in bronchi, bronchioles and
alveoli ->
• Increased mucus production and impaired ciliary motility in the large airways
• recruitment of neutrophils in smaller airways which release proteinases and
destroy collagen and elastin producing dilated alveoli
• A gradual decline in FEV1 with dyspnea only after FEV1 < 50%
• Recurrent pneumonia and function diminishes with each infection
Obstructive Lung Disease
• On PFTs patients with emphysema will have low FEV1 and FEV/VC and
increased TLC and RV
• Unlike patients with asthma, these patients will generally also have decreased
VC due to permanent destruction of small airwarys
• CXR initially normal but later shows hyperinflation, decreased vascular
markings and eventually signs of pulmonary HTN
Obstructive Lung Disease
Symptoms of COPD
• Pt typically presented with either:
• chronic productive cough,
• dyspnea or
• recurrent pneumonia.
• Intermittently the patient will develop increased cough, worsening
dyspnea or fever signifying COPD flair or exacerbation
Signs of COPD
• Inspection - “barrel chest” = increased AP diameter; wasting; use of
accessory MM
• Percussion - hyperressonance
• Auscultation - markedly decreased breath sounds; prolonged
expiratory phase; occasional wheezes or coarse crackles
• If severe or COPD flair then tachypnea, retractions, cyanosis, pursed
lip breathing (‘auto-PEEP’), and signs of right heart failure.
Diagnosis of COPD
• The definitive diagnosis of COPD is made on the basis of PFTs
(pulmonary function tests)
• In the absence of PFTs, a presumptive diagnosis can be made with:
• History of smoke exposure,
• Physical examination and
• CXR.
Diagnosis of COPD
Differential Diagnosis
• ARDS (Acute respiratory distress syndrome)
• Aspiration pneumonia and pneumonia
• Heart Failure
• Bacteria pneumonia
• Pulmonary Embolism
• Myocardial Infarction
• Pneumothorax
Investigation
• FBP
• ABG (arterial blood gas)
• Serum electrolyte
• Pulse oximetry
• Electrocardiography
• Pulmonary Function Tests
• Imaging (chest x-ray)
CXR of COPD
Treatment of COPD - Acute
• O2 for goal saturation 90% (not higher)
• Watch for signs of hypercarbia.
• Inhaled Ipratoprium
• Oral Steroids x 2-4 weeks
• Antibiotics (Ciprofloxacin)
Treatment of COPD - chronic
• Assist patient to quit smoking!
• Preparation - counsel and set a quit date
• Nicotine replacement or nortryptilline
• Trial of prn salbutamol.
• Inhaled steroids to prevent progression.
• Home oxygen if O2 saturation < 85%.
• Physiotherapy to increase respiratory muscle strength.
Pathophysiology of Smoking
• Tobacco contains nicotine, carcinogens and other toxins (including
CO)
• Burning tobacco (as with cigarettes) causes aeresolization of nicotine
and tar which is then absorbed through alveoli.
• Within 1-2 years lung function begins to decline
• With chewing and pipe/cigar smoking, nicotine and tar are absorbed
in the mouth
Risks of Smoking
• 40% of smokers will die of some complication of smoking
• … but cessation of smoking:
• Decreases rates of CV event in 6-12 months (likely due to platelet function)
• Although it takes 15 years until risk resolves
• Improves respiratory function and cough
• Reduces risk of cancer
Smoking, COPD and
genetics
Other risks of smoking
Pack year
• Is a term used to describe the number of cigarettes a person has
smoked overtime. One pack year is defined as 20 manufactured
cigarettes (one pack) smoked per day for one year.
Pack-Years
• Risk of smoking related disease is related to:
• Genetics
• Total number of cigarettes smoked.
• For these reason we calculate the smokers pack-years of smoking.
Calculation
= packs smoked/day x years smoked
• Example # 1: 1/2 pack/day x 10 years = 5 pack years smoked
NB: 1 pack = 20 cigarettes
Example #2: pt smoked 15 cigarette a day for 40 year. How many pack-year smoking
history.
Cont…..
Soln: 15cigarete/20 total cigarette per packx40yrs =30pack-year smoking history
• Quit date. For example, risk of CV event seems to return to normal 5 years
after smoking.
Pack-Years
Smoking in Africa
• Rates of smoking are increasing throughout Africa, especially in urban
areas and amongst teenagers.
• In Jburg - 60% of male laborers smoke.
• In Uganda - 33% of male secondary students smoke.
• Currently M>>F but smoking seems to be increasing in females as well
 Smoking in Africa

As Africans earn more money, they will likely smoke more…

Smoking Cessation
Smoking Cessation
Smoking Prevention
• Persuade your friends, family and patients not to smoke!
• Kumbuka, “kuzuia ni bora kuliko tiba.”
Bronchitis

YASIN M, MD
Introduction
• Bronchitis is one of the top conditions for which patients
seek medical care.
• Bronchitis is characterized by inflammation of the
bronchial tubes (or bronchi), which are the air passages
that extend from the trachea into the small airways and
alveoli.
• Triggers may be infectious agents, such as viruses or
bacteria, or non-infectious agents, such as smoking or
inhalation of chemical pollutants or dust.
Cont…
There two types of bronchitis, namely acute and
chronic bronchitis.
• Acute bronchitis is manifested by cough and,
occasionally, sputum production that last for not more
than 3 weeks.
• Chronic bronchitis is defined clinically as the presence
of a cough productive of sputum not attributable to
other causes on most days for at least 3 months over 2
consecutive years.
 Aetiology of Acute Bronchitis
• Acute bronchitis was defined as an acute self-limited lower
respiratory tract infection manifested predominantly by cough
with or without sputum production, lasting no more than 3
weeks with no clinical or any recent radiographic evidence to
suggest an alternative explanation.
• In acute bronchitis some isolated virus(influenza A and B
viruses,
parainfluenza virus, respiratory syncytial virus, coronavirus,
adenovirus, and rhinovirus) and
bacteria (Bordetella pertussis, Chlamydophila (Chlamydia)
pneumoniae, and Mycoplasma pneumonia).
• Respiratory viruses are the most common causes of acute
bronchitis
Cont…
• Other infections
Mycoplasma species
Chlamydia pneumoniae
Streptococcus pneumoniae
Moraxella catarrhalis
Haemophilus influenzae
Cont…
• Exposure to irritants, such as pollution, chemicals, and
tobacco smoke, may also cause acute bronchial
irritation
Risk Factor for Chronic Bronchitis
1.Cigarette smoking
2.Indoor air Pollution : Exposure from burning woods
3.Occupational exposure : Coal miners >Tunnel Workers >Hard-rock
miners >Concrete manufacture>Livestock farming (i.e. to pesticides)
4. Exposure to agricultural products
5. Use of domestic solid fuel
Aetiology of Chronic Bronchitis
• Cigarette smoking is indisputably the predominant
cause of chronic bronchitis.
Estimates suggest that cigarette smoking accounts for
85-90% of chronic bronchitis and chronic obstructive
pulmonary diseases (COPD).
Studies indicate that smoking pipes, cigars, and
marijuana causes similar damage.
Cont…

Smoking impairs ciliary movement, inhibits the

function of alveolar macrophages, and leads to
hypertrophy and hyperplasia of mucus-secreting
glands.
Smoking can also increase airway resistance via
vagally mediated smooth muscle constriction.
Unless some other factor can be isolated as the
irritant that produces the symptoms, the first step
in dealing with chronic bronchitis is for the patient
to stop smoking.
Cont…
• Bacterial or viral infections
• Environmental pollution
Epidemiology of Bronchitis
• Although found in all age groups, acute bronchitis is
most frequently diagnosed in children younger than 5
years.
• Whereas chronic bronchitis is more prevalent in people
older than 50 years.
• Bronchitis affects males more than females
Cont…
• Bronchitis occurs more frequently in
Populations with a low socioeconomic status
People who live in urban and highly industrialized areas
• No difference in racial distribution has been reported
 Clinical Features of Bronchitis
Clinical presentation
• Patients with acute bronchitis present with a cough lasting more than five days
(typically one to three weeks), which may be associated with sputum production.
• Cough in the absence of fever, tachycardia, and tachypnoea suggests bronchitis,
Symptom of Acute Bronchitis
• Cough is the most commonly observed symptom;
generally lasts from 10-20 days
• Purulent sputum is reported in 50% of persons with
acute bronchitis
• Sore throat
• Runny or stuffy nose
• Headache
Cont…
• Muscle aches
• Extreme fatigue
• Fever is a relatively unusual sign and, when
accompanied by cough, suggests either
influenza or pneumonia.
• Nausea, vomiting, and diarrhoea are rare.
Cont…
• Severe cases may cause general malaise and chest
pain.
• With severe tracheal involvement, burning, substernal
chest pain associated with respiration, and coughing
may occur.
• Dyspnea and cyanosis are not observed in adults unless
the patient has underlying COPD or another condition
that impairs lung function
Signs of Acute Bronchitis

• Conjunctivitis, adenopathy, and rhinorrhea suggest

adenovirus infection
• Inspiratory stridor may occur
• Localized lymphadenopathy
• Rhinorrhea to coarse rhonchi
• Use of accessory muscles can be observed in
severe cases
• Pharyngeal erythema may or may not be present
Chronic Bronchitis
It defined by a chronic productive cough for three months
in each of two successive years in a
patient in whom other causes of chronic cough have been
excluded. Patients may get secondary
bacterial infection with development of fever and
production of thick smelly sputum

SYMPTOMS OF CHRONIC BRONCHITIS

• Onset is typically in the fifth decade
• Productive cough
• A morning ‘smoker's cough’ is frequent, usually
mucoid in character but becoming purulent during
exacerbations, which in early disease are
intermittent and infrequent.
Cont…
• Volume is generally small. Production of more than 60
mL/d should prompt investigation for bronchiectasis
• Wheezing may be present but does not indicate severity
of illness
• As chronic bronchitis progresses, exacerbations become
more severe and more frequent.
Cont…
• Gas exchange disturbances, worsen and dyspnea
becomes progressive
• Exercise tolerance becomes progressively limited
• With worsening hypoxemia, erythrocytosis and cyanosis
may occur
• The development of morning headache may indicate
the onset of significant CO2 retention
Cont…
• In advanced disease, weight loss is frequent and
correlates with an adverse prognosis
• When blood gas derangements are severe, cor
pulmonale may manifest itself by peripheral oedema
and water retention
Signs of Chronic Bronchitis
• The physical examination has poor sensitivity and
variable reproducibility in chronic bronchitis.
• Findings may be minimal or even normal in mild
disease, requiring objective laboratory data for
confirmation.
• In early disease, the only abnormal findings may be
wheezes on forced expiration and a forced expiratory
time prolonged beyond 6 s.
Cont…
• With progressive disease, findings of hyperinflation
become more apparent.
• These include an increased anteroposterior diameter of
the chest, decreased cardiac dullness, and distant heart
and breath sounds.
• Coarse inspiratory crackles and rhonchi may be heard,
especially at the bases
Cont…
• Breathing through pursed lips prolongs expiratory time
and may help reduce dynamic hyperinflation.
• Cor pulmonale and right heart failure may be evidenced
by dependent oedema and an enlarged, tender liver.
• Cyanosis is a somewhat unreliable manifestation of
severe hypoxemia and is seen when severe hypoxemia
and erythrocytosis are present.
Differential Diagnosis of Acute Bronchitis
• Asthma
• Pneumonia
• Bronchiectasis
• Chronic bronchitis
• Pharyngitis
• Sinusitis, acute
Differential Diagnosis of Chronic
Bronchitis
• Bronchiectasis
• Tuberculosis
• Congestive heart failure
Investigations at Dispensary/Health Centre
• Obtain a complete blood count with differential
• A sputum sample showing neutrophil granulocytes
(inflammatory white blood cells)
• Gram stain and Ziel Neilsen stain
 Investigation at Hospital Level
• A chest X-ray that reveals hyperinflation Some conditions that predispose to
bronchitis may be indicated by chest radiography.
• A sputum sample showing neutrophil granulocytes (inflammatory white blood
cells) Gram stain and Ziel Neilsen stain, culture showing that has pathogenic
microorganisms such as Streptococcus spp. )
• FBP
• ESR /CRP OR Procalcitonin
• Serum alpha-1 antitrypsin levels
• Chest radiography (if the patient is elderly or physical findings suggest
pneumonia)
• Sputum cytology (if the cough is persistent)
• Blood culture and microbial sensitivity (if bacterial super-infection is suspected)
• Bronchoscopy (to exclude foreign body aspiration, tuberculosis, tumours, and
other
• chronic diseases and patient with worsening symptoms)
• Lung function Test (Spirometry and Peak expiratory flow rate)
 Treatment of Acute Bronchitis
• Therapy is generally aimed toward alleviation of symptoms.
• Care for acute bronchitis is primarily supportive and should
ensure that the patient is oxygenated adequately.
• In acute bronchitis, treatment with beta2-agonist
bronchodilators may be useful in patients who have
associated wheezing with cough and underlying lung
disease.
Symptomatic Treatment
• With non-steroidal anti-inflammatory drugs: paracetamol, acetyl salicylic acid
• Cough management refer section 9.1.1
• There is NO benefit from antibiotic use in acute bronchitis.
• Discourage smoking and other irritating factors
 Treatment of Chronic Bronchitis
Treatment of chronic bronchitis is based on
• The principles of prevention of further evolution of disease
• Preservation of airflow
• Preservation and enhancement of functional capacity
• Management of physiologic complications
• Avoidance of Acute exacerbationsSmoking cessation
• Elimination of tobacco smoking confers significant survival
benefit to patients with chronic bronchitis
 Cont…
Non-pharmacological Treatment
• Stop smoking (Reducing loss of lung function) and/or remove from
hazardous environment
• Prompt treatment of infective exacerbations
• Controlled oxygen therapy
• Physiotherapy
• Pulmonary Rehabilitation (consist of education, lifestyle modification,
regular physical
activities, physiotherapy and avoid indoor and outdoor pollutants)
• Nutrition support
• BIPAP in specialized center
• Influenza vaccine in specialized center
Cont…
Bronchodilators
• These drugs improve dyspnea and exercise tolerance
by improving airflow and by reducing end-expiratory
lung volume and air-trapping.
• Bronchodilator medication is available in metered-
dose inhaler (and some dry-powder inhalers) and in
nebulizable and oral forms.
• Inhalers deliver medications directly to the airways
and have limited systemic absorption and side
effects.
 Cont…
• Salbutamol (short acting beta 2 agonist).
• Acute symptoms: 2 inhalations repeated 6 hourly
• Other bronchodilators include Theophylline
NOTE
Pharmacological Treatment
• Pharmacologic therapy for Chronic Bronchitis is directed towards 3 major
goals
• Relieving symptoms during stable disease
Cont…
Glucocorticoids
• Chronic bronchitis is a disease associated with airway
inflammation; therefore, glucocorticoids are an
intuitively attractive therapeutic modality.
• Long-term systemic glucocorticoid use is associated
with multiple side effects. In particular, they have been
associated with worsened osteoporosis and increased
risk of vertebral fracture.
Cont…
• If systemic steroids are used, the lowest effective dose
should be employed and alternate day dosing used
whenever possible, e.g. prednisolone.
• The use of inhaled glucocorticoids ameliorates systemic
side effects. Examples include
Beclomethasone dipropionate
504-840200 mcg (4puffs) twice daily or 100mcg (2 puffs) 3 – 4
times daily by aerosol inhalation/d (42 mcg per actuation, 12-20
puffs qid) inhaled PO divided tid/qid
Oxygen Therapy
• Severe and progressive hypoxemia is often seen in
advanced chronic bronchitis and may result in cellular
hypoxia with deleterious physiologic consequences.
• Long-term O2 therapy has been shown to reverse
secondary polycythemia; improve body weight;
ameliorate cor pulmonale; and enhance
neuropsychiatric function, exercise tolerance, and
activities of daily living.
Cont…
• Oxygen is most frequently delivered through a nasal
cannula at rates of 2 to 5 L/min.
Note: Most of the treatment options might not be present
at the primary health care levels (dispensary and health
centre) and therefore referring the patient to hospitals for
proper management will be unavoidable.
Mucoactive Agents-Reduced overproduction and hypersecretion, increases
elimination
For pharmaceutical management; refer to emergency and critical care chapter
Hypertonic saline-stimulate productive cough and decreases sputum
viscoelasticity, increases mucociliary clearance.
7% hypertonic saline or 0.9% saline bd for PRN
Bronchodilators (Beta-agonists)-Promotes mucus clearance by increasing
airway luminal
diameter and ciliary beat frequency, reduces hyperinflation, improve PEF
A: SABA: Salbutamol (Inhalation) 100µg 2puff 6hourly
OR
LABA: salmeterol+fluticasone or in combination with steroids
(salmeterol+fluticasone or budenoside fluticasone)
Muscarinic antagonists -Decrease contractility of smooth muscle in
the lung, inhibits bronchoconstriction and mucus secretion
SAMA: S: ipratropium bromide (aerosol) 20–80mcg, 6–8 hourly
LAMA: S: tiotropium (mist inhaler) 6mcg 2puff 24hourly Preventing
exacerbations
Home Therapy

• For patients with mild exacerbations for whom

outpatient therapy is appropriate, a combination of
anticholinergic and short-acting b2-adrenergic
agonist bronchodilators should be prescribed.
• The presence of increased sputum volume or
purulence suggests an infectious cause of an
exacerbation. With either of these features is
present in conjunction with increased
breathlessness or when both are present,
antibiotics should be prescribed.
Cont…
• The organisms most frequently associated with mild
chronic bronchitis exacerbations include Streptococcus
pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis.
Common drugs used are
• Trimethoprim/sulfamethoxazole (cotrimoxazole) 960 mg
PO 12 hourly for 10-14 days
Cont…
• Doxycycline 100 mg PO bid for 10 days.
• Amoxicillin and clavulanate 500 mg PO 8 hourly for 7-10 d; not to
exceed 2 g/d
Hospital Management
• Hospitalized patients should receive bronchodilators,
antibiotics, oral glucocorticoids, and sufficient O2 to
keep the SaO2 > 90%. β2-agonists and anticholinergic
agents should be given together every 4 to 6 hours.
Cont…
Note: In absence of oxymeter indication for oxygen
therapy will depend on clinical grounds based on signs
like: dyspnoea, tachypnoea and cyanosis Note that all
patients who need admission/hospitalization need to be
referred
THANKS FOR
LISTENING
Emphysema
STANDARD TREATMENT GUIDELINES
Emphysema
It is a destructive process in the gas-exchanging air spaces of the lung that results in
perforations, obliteration of airspace walls, and coalescence of small distinct airspaces into
much larger ones, leading to enlargement of the gas exchanging units of the lungs. These
changes cause loss of elastic recoil of the lungs and abnormal gas exchange.
Clinical presentation
• Shortness of breath,Cough, sometimes caused by the production of mucus,Wheezing
• Slow and prolonged expiration ,Chest wall hyperinflation,
• Limited diaphragmatic motion on auscultation,Distant breath sounds, and heart sounds
• Coarse early inspiratory crackles.
• Use of accessory muscles
• Pursed-lip breathing
Signs of cor pulmonale. (Raised JVP, peripheral oedema,hepatomegaly etc)
• Cyanosis
• Asterixis
Investigations
• Haematocrit(men>52% and >47men) Or FBP (look at haematocrit)
• ABG(look for bicarbonate-metabolic alkalosis)
• CXR
• Sputum culture and Microbial sensitivity
• Pulmonary function tests
• Six minutes’ walk test
• CT SCAN OF THE CHEST/HRCT
(for evaluation for Lung Volume
Reduction Surgery)
Non-pharmacological Treatment:
• Stop smoking
• Give oxygen after evaluation
Pharmacological Treatment
Inhaled bronchodilators relax and open the airways. They may be short-acting (albuterol,
ipratropium) or long-acting (salmeterol, tiotropium,). These medicines may be available as inhalers
("puffers") or as a solution.
Bronchiecta
sis

By
YASIN M, MD
Introduction
• Bronchiectasis is an abnormal and permanent
dilatation of bronchi, most often secondary to an
infectious process.
• It may be either focal, involving airways supplying a
limited region of pulmonary parenchyma, or diffuse,
involving airways in a more widespread distribution.
Bronchiectasis OR
• Bronchiectasis is a progressive respiratory disease
characterized by permanent dilatation of the bronchi
and associated with a clinical syndrome of cough,
sputum production and recurrent respiratory
infections.
Cont…
• Although this definition is based on pathologic
changes in the bronchi, diagnosis is often
suggested by the clinical consequences of
chronic or recurrent infection in the dilated
airways and the associated secretions that pool
within these airways.
Aetiology and Pathogenesis
• Bronchiectasis is a consequence of inflammation
and destruction of the structural components of
the bronchial wall.
• Infection is the usual cause of the inflammation .
Cont…
Infectious Causes
• Adenovirus and Influenza virus are the main viruses that
cause bronchiectasis in association with lower
respiratory tract involvement.
• Virulent bacterial infections, especially with potentially
necrotizing organisms such as Staphylococcus aureus,
Klebsiella, and anaerobes, remain important causes of
bronchiectasis when antibiotic treatment of pneumonia
is not given or is significantly delayed.
Cont…
• Bronchiectasis has been reported in patients with HIV
infection, perhaps at least partly due to recurrent
bacterial infection.
• Tuberculosis can produce bronchiectasis by a
necrotizing effect on pulmonary parenchyma and
airways and indirectly as a consequence of airway
obstruction from bronchostenosis or extrinsic
compression by lymph nodes.
Cont…
Others causes include
• Non Tuberculous mycobacteria
• Mycoplasmal (rare)
• Fungal infections (rare)
Predisposing Factors (to Recurrent/Chronic
Infections and hence Bronchiectasis)
Endobronchial obstruction leads to local impairment of
host defense mechanisms predisposing to recurrent
infections.
• Slowly growing endobronchial neoplasms
• Foreign-body aspiration
• Broncho stenosis, from impacted secretions, or from
extrinsic compression by enlarged lymph nodes.
Cont…
Generalized impairment of pulmonary defense
mechanisms occurs with
• Immunoglobulin deficiency
• Primary ciliary disorders
• Cystic fibrosis
Cont…
Non-infectious Causes
• Exposure to a toxic substance that incites a severe
inflammatory response. Examples include inhalation of
a toxic gas such as ammonia or aspiration of acidic
gastric contents
• An immune response in the airway may also trigger
inflammation, destructive changes, and bronchial
dilatation.
Epidemiology of Bronchiectasis
• Frequency
No systematic data are available to detail the
incidence or prevalence of bronchiectasis.
Bronchiectasis remains a major cause of morbidity in
less-developed countries, especially in countries with
limited access to medical care and antibiotic therapy.
Cont…

• Race
No racial predilection exists other than those that may
be associated with socioeconomic status.
• Sex
Evidence suggests that non – Cystic Fibrosis-related
bronchiectasis is more common and more virulent in
women, particularly slender white women older than 60
years.
In these patients, bronchiectasis is often caused by
primary Mycobacterium avium complex (MAC) infection
Cont…
• Age
In the pre antibiotic era and in today's less-developed
countries, symptoms usually began in the first decade of life.
Today, the age of onset, except for those with Cystic Fibrosis,
has moved into adulthood.
The differences in prevalence between age groups are a direct
reflection of the differences in prevalence of the underlying
causes of bronchiectasis, lung disease, and/or chronic
infections
Clinical Manifestations of Bronchiectasis

History
• Patients typically present with persistent or
recurrent cough and purulent sputum production
which is postural related.
• Hemoptysis occurs in 50 to 70% of cases
• When a specific infectious episode initiates
bronchiectasis, patients may describe a severe
pneumonia followed by chronic cough and sputum
production.
• Alternatively, patients without a dramatic initiating
Cont…
• Dyspnea or wheezing generally reflects either
widespread bronchiectasis or underlying chronic
obstructive pulmonary disease.
• With exacerbations of infection, the amount of sputum
increases, it becomes more purulent and often more
bloody, and patients may become febrile.
Physical Examination
• Variable
• Any combination of crackles, rhonchi, and wheezes may
be heard, all of which reflect the damaged airways
containing significant secretions.
• As with other types of chronic intrathoracic infection,
clubbing may be present.
Cont…
• Cyanosis and plethora
• Wasting and weight loss
• Patients with severe, diffuse disease, particularly those
with chronic hypoxemia, may have associated cor
pulmonale and right ventricular failure.
Differential Diagnosis of Bronchiectasis

• Bronchial asthma
• Chronic Bronchitis
• Acute Bronchitis
• Emphysema
• Aspiration Pneumonia/ Bacterial Pneumonia
• Pulmonary Tuberculosis
 Diagnosis
Radiographic and Laboratory Findings
• Chest Radiograph
Is important but the findings are often nonspecific
The radiograph may be normal with mild disease
• Computed tomography (CT)-in advanced centres
Provides an excellent view of dilated airways as seen in cross-
sectional images
INVESTIGATIONS
FBP, ESR, Serum IgE and IgE to aspergillus, serum immunoglobulin
(IgG, IgA, IgM) CXR, Sputum
culture and sensitivity, CT-Chest (CT contrast if suspicion of PE/HRCT,
bronchoscopy.
Cont…
• Sputum Examination
Often reveals an abundance of neutrophils and
colonization or infection with a variety of possible
organisms.
Appropriate staining and culturing of sputum often
provide a guide to antibiotic therapy.
Cont…
Other investigation (to determine the cause) in advanced
centres
• Fiberoptic bronchoscopy for endobronchial obstruction
• Measurement of sweat chloride levels for cystic fibrosis
• Skin testing, serology, and sputum culture for
Aspergillus
• Pulmonary function tests may demonstrate airflow
obstruction associated with chronic obstructive lung
disease.
Non-pharmacological Treatment
• Physiotherapy and postural drainage
• Avoid smoking
• Airways clearance technique
• Pulmonary rehabilitation
• Respiratory care during childhood measles helps prevent the development of bronchiectasis in children
Pharmacological Treatment
Consider antibiotics in patients with bronchiectasis with >3 exacerbations per year. (empirical
treatment while wait for culture and sensitivity)
Adults:
A: ciprofloxacin (PO) 500mg 12hourly for 10days AND A: metronidazole (PO) 400mg 8hourly for 10days
Children:
A: amoxicillin (PO) 40mg/kg in 2 divided doses for 7days AND A: metronidazole (PO) 7.5 mg/kg 8hourly for
5–7days (If pseudomonas aeruginosa suspicion (should be culture guided)
D: ceftazidime (IV) 2g 8hourly for 14days
Cont…
Therapy has four major goals
• Elimination of an identifiable underlying problem
• Improved clearance of tracheobronchial secretions
• Control of infection, particularly during acute
exacerbations
• Reversal of airflow obstruction
Cont…
General Therapy
• Patients should stop smoking
• Patients should avoid second-hand smoke
• Patients should have adequate nutritional intake with
supplementation, if necessary
Cont…
• Immunizations for influenza and pneumococcal
pneumonia are recommended
• Immunizations for measles, rubeola, and pertussis
should be confirmed
• Oxygen therapy is reserved for patients who are
hypoxemic with severe disease and end stage
complications, such as cor pulmonale
Cont…
Bronchial Hygiene
• With its tenacious sputum and defects in clearance of
mucus, good bronchial hygiene is paramount in the
treatment of bronchiectasis.
• Postural drainage with percussion and vibration is used
to loosen and mobilize secretions.
Cont…
Antibiotics
• Antibiotics are the mainstay of treatment.
• The route of antibiotic administration varies with the
overall clinical condition, with most patients doing well
on outpatient regimens.
• Some patients benefit from a set regimen of antibiotic
therapy, such as therapy for 1week of every month.
Cont…
• The choice of antibiotic is provider dependent, but in
general the antibiotic chosen should have a reasonable
spectrum of coverage, including the most common
Gram-positive and Gram-negative organisms.
Cont…
• Treatment of the patient who is more ill or the patient
with Cystic Fibrosis often requires intravenous anti-
Pseudomonas species coverage with an aminoglycoside,
most often in combination with an antipseudomonal
synthetic penicillin or cephalosporin
• In acute exacerbation, broad-spectrum antibacterial
agents are generally preferred.
Cont…
• However, if time and the clinical situation allows, then
sampling respiratory secretions during an acute
exacerbation may allow treatment with antibiotics
based on specific species identification.
Cont…
Acceptable choices for the outpatient who is mild
to moderately ill include;
• Amoxicillin: 500 mg PO 8 hourly for 10 days
• Doxycycline: 100 mg PO every 12 hours for 10 days
• Trimethoprim-sulfamethoxazole 960mg PO 12 hourly for
10 days
Cont…
• A newer macrolide
Azithromycin: Day 1: 500 mg PO; Days 2-5: 250 mg/d PO
Clarithromycin 500 mg PO bid for 7-14 days
• A second-generation cephalosporin
• One of the fluoroquinolones e.g. Levofloxacin 500 mg
PO/IV once daily
• In general, the duration is 7-10 days
Cont…
For patients with moderate-to-severe symptoms,
parenteral antibiotics are indicated
• An aminoglycoside
Gentamicin: 3 mg/kg/d IV divided tid in normal renal
function; once-a-day dosing also effective
Amikacin: 10-15 mg/kg/d IV/IM divided bid/tid; not to
exceed 1.5 g/d regardless of higher Body Weight
Cont…
• An antipseudomonal synthetic penicillin(If pseudomonas aeruginosa
suspicion (should be culture guided)
D: ceftazidime (IV) 2g 8hourly for 14days
• A third-generation cephalosporin
Ceftriaxone: IV 1-2g bid OR
S: piperacillin+tazobactam (FDC) (IV) 4.5mg 8hourly for 14days
AND
D: itraconazole (PO) 100mg-200mg 12hourly

• For Prevention of infection

A: ciprofloxacin 500mg (PO) 24hourly for 7–14days OR
A: erythromycin (PO) 250–500mg 24hourly for 7–14days
Cont…

Bronchodilators
Bronchodilators, including beta-agonists and anti-
cholinergics, may help some patients with
bronchiectasis, presumably reversing
bronchospasm associated with airway
hyperreactivity and improving mucociliary
clearance
• Salbutamol (short acting beta 2 agonist)
Acute symptoms: 2 inhalations repeated q4-6h
• Salmeterol (Long acting beta 2 agonist)

Anti-inflammatory Medication
• The rationale is to modify the inflammatory response caused by the microorganisms
associated with bronchiectasis and subsequently reduce the amount of tissue damage.
• A practical approach is to use tapering oral corticosteroids (e.g. prednisolone) and
antibiotics in the acute exacerbation and to consider inhaled corticosteroids for daily
use in patients with significant obstructive physiology on pulmonary function testing
and evidence of reversibility suggesting airway hyperreactivity.
Cont…
• Beclomethasone dipropionate
200 mcg (4puffs) twice daily or 100mcg (2 puffs) 3 –
4 times daily by aerosol inhalation
Cont…
Surgical Therapy
• When bronchiectasis is localized and the morbidity is
substantial despite adequate medical therapy, surgical
resection of the involved region of lung should be
considered.
Complications

• Recurrent pneumonia requiring hospitalization

• Empyema
• Lung abscess
• Hemoptysis
Cont…
• Progressive respiratory failure
• Cor pulmonale
• Progressive respiratory failure and cor pulmonale
are the most common causes of pulmonary-
related mortality in bronchiectasis.
Prognosis

• Overall, the prognosis is good, but it varies with the

underlying or predisposing condition.
• Bronchiectasis associated with Cystic Fibrosis may carry
a worsened prognosis.
• In general, patients do well if they are compliant with all
treatment regimens and practice routine preventive
medicine strategies.
• Overall, the prognosis is good, but it varies with the
underlying or predisposing condition.
THANKS FOR LISTENING
Pulmonary
embolism(
PE)
By dr. sawe
Learning objectives
• Definition
• Risk factors and etiologies
• Clinical features
• Complications
• Clinical assessment
• Diagnosis
• Investigations
• Treatments
• Follow up
• Referral indications
• Preventive measures
Definition
• PE refers to obstruction of the pulmonary artery or one of its
branches by materials (eg thrombus, tumor, air, amniotic fluid,
bacteria and fat ) that originate else where in the body.
• Usually PE arises from a thrombus that originate in the deep venous
system of the lower extremities.
Risk factors
• Immobilization
• Surgery and trauma
• Pregnancy
• Oral contraceptives and estrogen replacement
• Malignancies
• Hereditary factor eg protein C ans S deficiency, antithrombin 3
deficiency etc.
• Acute medical illness eg HIV, CCF, SLE, MI, and Polythcemia
• Venous stasis
Etiology
• Virchow's triad proposes that the VTE pathogenesis is a result of:
o Alterations in blood flow (ie, stasis)
o Vascular endothelial injury
o Hypercoagulability (inherited or acquired)
• VTE often arise from synergistic effects of multiple risk factors, e.g a
patient with inherited factor V Leiden mutation uses oral
contraceptives (acquired risk on genetic risk background)
• A risk factor for thrombosis identified in over 80% of patients VTE
Cont…..
Clinical features
• PEs are frequently asymptomatic
• Symptomatic patients most commonly present with dyspnea
• Signs of DVT are only found in about 1/3 of PE patients
Cont……
• Dyspnoea
• Pleuritic chest pain
• Productive cough
• Hemoptysis
• Seizures
• Reduced level of consciousness etc.
Clinical assessment
• On general examination
+/- decreased LOC, tachypnoea, tachycardia, +/- fever, hypotension,
+/- cyanosis.
• On RSE
Rales localized, wheeze, decrease breath sound, Pleural friction rub,
signs of pleural effusion (stony dullness on percussion, decreased
fremitus).
• On CVS exam
Parasternal heave, loud P2, increased JVP
Complications
• Obstructive shock
• Atrial and ventricular arrhythmias
• Cor pulmonary
• Lung infarctions
• Right to left intracardiac shunt
• Paradoxical embolism
• Pleural effusions
• Pulseless electrical activities
• Secondary pulmonary arterial hypertension
Diagnosis
• Diagnosis is based on history and physical examination, and
confirmed with investigastions which will be discussed on the next
session
• The Wells criteria also can be used to determine risk (pretest
probability) of PE
Cont…
The Modified Wells criteria (PE)
Investigations
• Lab investigations:
FBP– to check for leukocytosis, erythrocytosis, thrombocytosis and
thrombocytopenia.
D-dimers---useful in low pretest probability when elevated
Troponin levels--- can rise in up to 50% of PE
ABG—rules out hypoxemia, hypocapnia, respiratory alkalosis etc.
BNP--- can rise in PE
Cont …..
• Radiological investigations
Pulmonary CT Angiogram or V:Q scan—this is the gold std to dx PE
CXR—can reveal atectasis, pleural effusion, parenchymal oparcities,
elevated hemidiaphragm, knuckle sign, +/- right side cardiomegaly, and
+/- pulmonary edema.
ECG---can show tachycardia, non specific ST-T wave abnormality, RBBB
etc ( note; unfortunately only 20% of patients with proven PE has the
classic ECG abnormalities).
ECHO---it can diagnose PE and rule out other diseases mistaken by PE
and rule out most of cardiac complications of PE.
Treatment
• The goals of treatment for VTE are
o Anticoagulation to prevent further clot generation and
o Thrombolysis if the thrombus is large enough to cause hemodynamic
compromise
Cont…
• Anticoagulation
Anticoagulation with parenteral (intravenous or subcutaneous)
and oral anticoagulants is the mainstay of VTE therapy
o Typically, one of the parenteral agents (e.g. heparin, LMWH, or fondaparinux) or a new oral
anticoagulant (e.g. rivaroxaban) is started first then transitioned to a traditional oral
anticoagulant (e.g. warfarin) for chronic anticoagulation
• Thrombolysis
Tissue plasminogen activator (tPA): activates plasminogen (Pg) to
plasmin (Pn), which cleaves the thrombus, generating soluble D-dimer
products
Cont…
• Anticoagulants used;
o Typically, one of the parenteral agents (e.g. heparin, LMWH, or fondaparinux) or a new oral
anticoagulant (e.g. rivaroxaban) is started first then transitioned to a traditional oral
anticoagulant (e.g. warfarin) for chronic anticoagulation.
• Options for long-term anticoagulation include oral anticoagulants (ie,
factor Xa inhibitors, direct thrombin inhibitors, and warfarin) and
parenteral subcutaneous anticoagulants (low molecular weight
[LMW] heparin and fondaparinux)
• While the factor Xa and thrombin inhibitors are typically preferred
Cont…
• Factor Xa inhibitors - rivaroxaban, apixaban, edoxaban and oral direct
thrombin inhibitors dabigatran– These oral agents are preferred
anticoagulant for most hemodynamically-stable, non-pregnant
patients who do not have severe renal insufficiency or active cancer
o Similar efficacy to Warfarin,
o Reduced need for monitoring
o Lower bleeding risk profile, when compared with warfarin
Cont…
• Warfarin – Warfarin is preferred anticoagulant for patients in whom
factor Xa or direct thrombin inhibitors are not available and for
patients with severe renal insufficiency
o Requires multiple office visits for INR monitoring
o Higher bleeding risk when compared with direct oral anticoagulant
o Antidotes for warfarin-related bleeding are more readily available
Cont…
• Low molecular weight (LMW) heparin – Subcutaneous LMW heparin
is an acceptable alternative for non-pregnant patients in whom oral
medications are not feasible (eg, malabsorption)
o It is the preferred therapy for DVT during pregnancy and for patients with
active malignancy
o Some experts also prefer this agent in those with liver disease since the
elevated INR in this population may not reflect the effect of warfarin
o Laboratory monitoring is not required
o They are contraindicated in patients with severe renal dysfunction (CrCl
<30 mL/minute)
NB// dosages of anticoagulants refer stg
Alternative if anticoagulants are
contraindicated
• Thrombectomy: If a large thrombus creates hemodynamic
compromise, and there are contraindications to thrombolysis, the clot
can be surgically removed or by interventional radiology
• Inferior vena cava (IVC) filter: Temporary IVC filters can be placed to
stop the movement of clots from the deep veins of the lower
extremity from travelling to the pulmonary vasculature
Follow up
1. Duration of treatment
• Duration — It is critical that the duration of anticoagulation therapy be
individualized according to the presence or absence of provoking events
and risk factors, risk for recurrence and bleeding as well as to the individual
patient preferences and values
• In general, the following applies:
Most patients with a first episode of venous thromboembolism (VTE;
provoked or unprovoked) should receive anticoagulation for a minimum
of three months.
Extending anticoagulation beyond three months is NOT routinely
considered in patients who have a provoked episode of VTE with the
following: transient risk factors, assuming the risk factor is no longer
present (eg, surgery, cessation of hormonal therapy), isolated distal
DVT, subsegmental or incidental pulmonary embolism (PE), or those
in whom the risk of bleeding is considered to be high
In select populations, anticoagulation is extended to 6 or 12 months
(eg, phlegmasia cerulea dolens, a persisting but reversible risk factor),
although the benefits of this are unproven
Cont…

2. Switching anticoagulants during therapy

• Interruptions should be limited especially during the first three
months of anticoagulation. However, anticoagulants may need to be
changed for medical reasons as well as for altered patient preferences
• Reasons for switching agents include:
o The development of renal insufficiency (prolongs the half-life of
LMWH, fondaparinux, and factor Xa and direct thrombin inhibitors [ie, direct
oral anticoagulants (DOACs)])
o Perceived burdens of laboratory testing for warfarin
o Poor compliance or difficulty with international normalized ratio (INR) testing
o Resolution of active cancer
o Pain or inflammation at injection sites
o Cost
o Need for repeated invasive procedures
o Recurrence despite therapeutic anticoagulation
Cont…
3. Monitoring
• All patients on anticoagulation should be monitored clinically for
o Therapeutic efficacy (recurrence)
o Bleeding
o Development of conditions that affect the half-life of the medications used (eg,
renal failure, pregnancy, weight gain/loss)
o Adverse effects of the medications (eg, skin necrosis, thrombocytopenia,
osteoporosis).
• Factor Xa and direct thrombin inhibitors - do not require routine
laboratory monitoring because laboratory parameters have not been
correlated with clinical endpoints
• Warfarin
o The most common laboratory test used to monitor warfarin is the prothrombin time
(PT) ratio, usually expressed as the international normalized ratio (INR)
o The goal INR is 2 to 3
o Once the anticoagulant effect and the patient's warfarin dose requirements are
stable, the INR should be monitored usually every three to four weeks throughout
the course of warfarin therapy
• Low molecular weight heparin and fondaparinux – These agents do not
require routine laboratory monitoring because laboratory parameters have
not been correlated with clinical endpoints (recurrence and bleeding)
Referral indications
• All suspected PE must be referred for further advanced medical
interventions
Preventions
• Prevent all risks of PE and VTE as much as possible.
Pulmonary Embolism
STANDARD TREATMENT GUIDELINES
Acute Pulmonary Embolism
Clinical Spectrum less than two weeks
• Sudden onset of dyspnoea often with unexplained anxiety (most
common)
• Pleuritic chest pain and haemoptysis
• Massive embolism: pleuritic chest pain, cyanosis, right heart failure and
shock. Minor emboli or pulmonary infarction may herald massive embolism
and must be treated vigorously
• About 90% of emboli are from proximal leg deep vein thromboses (DVTs)
or pelvic vein thromboses. DVTs are at risk for dislodging and migrating to
the lung circulation. Thus,termed as venous thromboembolism (VTE).
 Diagnostic Criteria

Determination pre-test probability of PE ;Use validated scoring system:

Wells Score
• Score > 6.0–High clinical probability proceeds with imaging test to confirm PE
and treat,
• Score 2.0 to 6.0–Moderate clinical probability; negative D–dimer, PE is
excluded and D–dimer positive, obtain imaging tests to confirm based on result
treat.
• Score < 2.0–Low clinical probability negative D–dimer, PE is excluded. Positive
D–dimer obtain imaging tests to confirm or rule out and based on result treat
Alternatively
• Score > 4–PE likely, d–dimer positive proceeds with diagnostic imaging to
confirm and treat PE.
• Score 4 or less–PE unlikely, consider d–dimer to rule out PE
Wells Score
VARIABLE SCORE

clinically suspected dvt 3.0 Points

alternative diagnosis is less likely than PE 3.0 Points

Tachycardia (heart rate > 100) 1.5 Points

Immobilization (≥ 3d)/surgery in previous four weeks 1.5 Points

History of DVT or PE 1.5 Points

Hemoptysis 1.0 Points

Malignancy (with treatment within six months) or 1.0 Points

palliative
• ECG – Not reliable test for diagnosis may be normal. However,
• Sinus tachycardia most common feature, acute right ventricular strain – i.e. right axis
shift,S1Q3T3 occurs in small percentage of cases, may develop acute bundle branch block –right
or left, may simulate right ventricular infarction, may develop arrhythmias – eg atrialfibrillation
• Arterial blood gases; not diagnostic, the pO2 decreased <60mmHg due ventilation/perfusion
mismatch. pCO2 decreased due to hyperventilation, pH increased but may decrease in shocked
patient
• D–dimer test – very sensitive blood test, but not specific. A negative test d–dimer test
excludes an embolus in majority of cases(best exclusive test to rule out PE when is negative)
• Chest X–ray – Not very reliable usually normal, diaphragm may be raised on affected area,
atelectasis may occur, peripheral wedge–shaped shadow & plural effusion
• Cardiac Echocardiography: Useful in diagnosis, features suggestive or support evidence of
massive embolus acute right ventricular strain
• Computer Tomography Pulmonary Angiogram Scan (CTPA); Useful can demonstrate the
presence and extent of proximal pulmonary emboli
• Pulmonary Angiography: Still gold standard investigation, may be necessary to establish
Non-pharmacological Treatment
• Administer O2 – maintain pO2 > 60mmHg,
• Treat shock
• Correct electrolyte & acid base abnormalities and arrhythmias
• Ventilate if patient in respiratory failure
Pharmacological Treatment
Anticoagulation
B: unfractionated heparin (UFH) (IV) 10,000units then maintenance infusion starts with
6,000U over 6 hours to keep PTT or clotting time 2–3times above baseline. PTT should be
performed 12hourly per lab instruction. OR
S: low molecular weight heparin (SC) 1mg/kg 12hourly for 24hours
Start warfarin after 24hours of heparin and continue post discharge for long–term. If the
aetiology
unknown may be for life, if aetiology is established at least for six months. Maintain INR
2.0–3.0
Thrombolytic (Fibrinolysis)
Indicated in proximal massive pulmonary emboli and haemodynamically unstable if no
contraindication exists
S: streptokinase (IV)250,000IU over 30minutes, then 100,000IU per hour for 24hours OR
S: alteplase (rtPA) (IV) 100mg over 2hours
Referral: All cases suspected of pulmonary embolus should be referred to a high level of care –
specialized hospital care with HCDU/ICU
Chronic Pulmonary Embolism
Chronic pulmonary embolism is mainly a consequence of incomplete resolution of acute
pulmonary
thromboembolism. Clinically symptoms and signs may be preceded by Acute Pulmonary
Embolism
for more than 2weeks.
Pharmacological Treatment
Long-term oral anticoagulation C:warfarin(PO) 2–10mg 24hourly
OR S: rivaroxaban (PO) 15-20mg 24hourly
Referral: All cases suspected of pulmonary embolism should be referred to a high level of care
Hyperten
sion
By YASIN M, MD
Introduction
Hypertension
• Defining abnormally high blood pressure is extremely difficult and
subjective.
• Because the risk to an individual patient may correlate with the
severity of hypertension, a classification system is essential for making
decisions about aggressiveness of treatment or therapeutic
interventions.
Cont…

• Hypertension may be either essential or secondary.

• Essential hypertension is diagnosed in the absence of
an identifiable secondary cause
• Approximately 95% of adults patients have essential
hypertension
• Secondary hypertension accounts for fewer than 5% of
the cases
Pathophysiology
• Arterial blood pressure is a product of cardiac output and
systemic vascular resistance.
• Determinants of blood pressure include factors that affect
both cardiac output and arteriolar vascular physiology.
Cont…
• Regulation of normal blood pressure is a complex process.
Although a function of cardiac output and peripheral
vascular resistance, both of these variables are influenced by
multiple factors.
Cont…
• The factors affecting cardiac output include sodium intake,
renal function, and mineralocorticoids; the inotropic effects
occur via extracellular fluid volume expansion and an
increase in heart rate and contractility.
Cont…
• Peripheral vascular resistance is dependent upon the
sympathetic nervous system, humoral factors, and local
autoregulation. The sympathetic nervous system produces
its effects via the vasoconstriction or the vasodilatation
effect.
Cont…
• The humoral actions on peripheral resistance are also
mediated by other mediators such as vasoconstrictors
(angiotensin and catecholamines) or vasodilators
(prostaglandins and kinins
• Autoregulation of blood pressure occurs by way of
intravascular volume contraction and expansion, as well as
by transfer of transcapillary fluid.
Classification of Blood Pressure
Classification of Blood Pressure for Adults ≥18 Years Old

Category Systolic Pressure, Distolic Pressure,

mmHg mmHg
Optimal <120 <80

Normal <130 <85

High normal (Pre- 130–139 85–89

Hypertension)
Cont…
Hypertension

Category Systolic Pressure, Diastolic Pressure,

mmHg mmHg
Stage 1 (mild) 140–159 90–99
Stage 2 (moderate) 160–179 100–109
Stage 3 (severe) ≥180 ≥110
Isolated systolic ≥140 <90
hypertension
Aetiology and Epidemiology
Primary/Essential Hypertension
• Accounts for about 90-95% of hypertension patients in a
general population
• The cause is always not known
Cont…
Secondary Hypertension
• Small percentage of patients (2-10%) have a secondary cause
 The following is a list of secondary
causes of hypertension;
Renal (2.5-6%)
• Renal parenchymal disease
• Polycystic kidney disease
• Urinary tract obstruction
• Renin-producing tumor
Cont….
Renovascular Hypertension (0.2-4%)
• Arteriosclerotic
• Fibromuscular dysplasia
Cont….
Vascular
• Coarctation of aorta
• Vasculitis
• Collagen vascular disease
Cont…
Endocrine (1-2%)
• Primary aldosteronism
• Cushing syndrome
• Pheochromocytoma
• Congenital adrenal hyperplasia
Endocrine… cont..
• Hyperthyroidism and hypothyroidism
• Hypercalcemia
• Hyperparathyroidism
• Acromegaly
Cont…
Neurogenic
• Brain tumour
• Bulbar poliomyelitis
• Intracranial hypertension (raised intracranial pressure)
• Pregnancy-induced Hypertension
Clinical Features
History
Detailed history should extract the following information
• Extent of target organ damage
• Assessment of patients' cardiovascular risk status
• Exclusion of secondary causes of hypertension
Cont….
• Patients may have undiagnosed hypertension for years
without having their blood pressure checked. Therefore, a
careful history of end organ damage should be obtained.
• History of cardiovascular risk factors includes
hypercholesterolemia, diabetes mellitus, and tobacco use
(including chewing tobacco).
Cont…
• Obtain a history of over-the-counter medication use, current
and previous unsuccessful antihypertensive medication
trials, and ethanol intake.
• The history and physical findings that suggest the possibility
of secondary hypertension are a history of known renal
disease, abdominal masses, anemia, and urochrome
pigmentation.
Cont…
• History of sweating, labile hypertension, and palpitations
suggests the diagnosis of pheochromocytoma.
• History of cold or heat tolerance, sweating, lack of energy,
and bradycardia or tachycardia may indicate hypothyroidism
or hyperthyroidism.
• History of weakness suggests hyperaldosteronism.
Cont...
• Kidney stones raise the possibility of hyperparathyroidism.
• The presence of papilledema and other neurologic signs
raises the possibility of increased intracranial pressure.
• A history of drug ingestion, including oral contraceptives and
sympathomimetics should be obtained.
Physical Examination
Assess body habitus, including weight and height,
• An accurate measurement of blood pressure is the key to
diagnosis. Several determinations should be made over a
period of several weeks.
• At any given visit, an average of 3 blood pressure readings
taken 2 minutes apart using a mercury manometer is
preferable.
Cont…
• Blood pressure should be measured in both the supine and sitting
positions, auscultating with the bell of the stethoscope.
• As the improper cuff size may influence blood pressure measurement,
a wider cuff is preferable, particularly if the patient's arm
circumference exceeds 30 cm.
• The patient should rest quietly for at least 5 minutes before the
measurement.
Cont…
• Palpation of all peripheral pulses should be performed.
• A careful cardiac examination is performed to evaluate signs
of left ventricular hypertrophy (LVH). These include
displacement of apex, a sustained and enlarged apical
impulse, and the presence of a 4th heart sound (S4)
Cont…
• The neck should be palpated for an enlarged thyroid gland,
and assess for signs of hypo/hyperthyroidism
• Examine abdomen for palpable kidneys as in polycystic
kidneys; and auscultate for abdominal bruit to rule out
renovascular disease
Cont…
• Palpation of peripheral arterial pulses for radio femoral delay
found in Coarctation of the Aorta
• Thorough physical examination and fundoscopy for possible
secondary hypertension and to rule out complications
(neurological, cardiac, retinal)
Laboratory Studies
• Most of the investigations in a hypertensive patient are done
at hospital level and therefore, referral of the patient is
important to assess the causes and or complications.
Cont…

Unless a secondary cause for hypertension is suspected, only the

following routine laboratory studies should be performed
• CBC count
• Serum electrolytes
• Serum creatinine
• Serum glucose or fasting glucose
• Urinalysis
Cont…
• Lipid profile
Total cholesterol
Low-density lipoprotein [LDL]
High-density lipoprotein [HDL]
Triglycerides)
• Thyroid hormones
Imaging Studies
• CXR
• Echocardiography: The echocardiography study may detect LVH more
frequently than electrocardiography. The main indication for limited
echocardiography is evaluation for end organ damage in a patient
with borderline high blood pressure.
• Therefore, the presence of LVH despite normal or borderline high
blood pressure measurements requires antihypertensive therapy.
Cont…
Advanced tests for selected patients are only done at specialized
hospitals to rule out secondary causes and complications as indicated
during thorough history taking and physical examination:
• Renal Ultrasound (Polycystic kidney disease or parenchymal renal
artery disease),
• Renal Isotope scan or Renal Angiography (Renovascular disease),
Cont…
• Urinary metanephrines and plasma or urinary catecholamines
(Pheochromocytoma),
• Urinary Cortisol and Dexamethasone suppression test (Cushing’s
Syndrome)
• Plasma Renin Activity and Aldosterone (Aldosteronism) etc.
Differential Diagnosis
• Coarctation of Aortic
• Hyperthyroidism
• Hyperaldosteronism
• Renal Artery Stenosis
• Aortic Dissection
Treatment of Hypertension
Non-pharmacological Approach
Recommendations to lower blood pressure and decrease
cardiovascular disease risk include the following
• Reduction of weight if overweight
• Limit alcohol intake
Cont….
• Increase aerobic activity (30-45 min most days of the week)
• Reduce sodium intake (salt)
• Stop smoking and reduce intake of dietary saturated fat and
cholesterol for overall cardiovascular health
Cont…
Pharmacological
• For the first time patient should be referred to the hospital level for
investigations and initiation of treatment then follow up may be even
done at dispensary or health Centre.
• However, this may not always be possible particularly in rural areas.
The clinician will then be required to initiate treatment and closely
follow up the patient until referral to higher level is possible.
Cont…
• Pre-hypertension (systolic 130-139, diastolic 80-89): No
antihypertensive drug is indicated.
• The choice of antihypertensive drug is guided by availability,
cost, response to treatment side effects, age, Black or
Caucasian patient and presence of other diseases such as
Diabetes mellitus, Asthma, Heart Failure.
Cont…
• The aim of drug treatment to reduce the risk of
complications of Hypertension should be carefully explained
to the patient and a plan for patient’s treatment (drug dose
titration, change of drug, combination of drugs) should be
agreed with the patient.
Antihypertensive Categories
Diuretics
• Cause diuresis, which decreases plasma volume and edema, thereby
decreasing cardiac output and blood pressure.
Hydrochlorothiazide
• Inhibits reabsorption of sodium in distal tubules, causing increased
excretion of sodium, water, potassium, and hydrogen ions.
• Dose: 25mg PO daily; may be increased (if necessary) to 50mg daily.
In elderly – start with 12.5mg daily
Diuretics cont…
Amiloride (Midamor)
• Possesses weak natriuretic, diuretic, and antihypertensive activity
• Dose:5-20 mg PO od
Contraindications:
• acute or chronic renal insufficiency, and evidence of diabetic
nephropathy
Cont…
Beta-adrenergic Blocking Agents
• Used to treat hypertension as initial agents or in combination
with other drugs (e.g. thiazides).
• ß-adrenoceptor antagonist (Atenolol, Metoprolol,
Propranolol)
Cont…
• Atenolol and metoprolol selectively block beta1-receptors
with little or no effect on beta2 types. Propranolol is a class II
antiarrhythmic, nonselective, beta-adrenergic receptor
blocker with membrane-stabilizing activity that decreases
automaticity of contractions.
Cont…
Dose:
• Atenolol: 50 mg PO od; increase to 100 mg/d, if necessary.
• Metoprolol: Initially, 100 mg/d PO daily. Maintenance 100-200mg
daily once a day or in 2 divided doses.
• Propranolol: 40-80 mg PO bid initial; increase to 160-320 mg/daily.
Cont…
Alpha/beta-adrenergic Blocking Agents
• Block alpha-, beta1-, and beta2-adrenergic receptor sites,
thus decreasing blood pressure.
• May reduce cardiac output and decrease peripheral vascular
resistance e.g. Labetalol, Carvedilol.
Cont…
• Labetalol: orally initially 100mg (50mg in elderly) twice daily
increased at 2 weeks interval to 200-400mg twice a day (max 2.4g
daily). IV injection 50mg over 1 minute (repeated after 5 minutes if
necessary). By IV infusion 2mg/minute until satisfactory response.
• Carvedilol: 12.5mg PO initially once daily, increase after 2 days to
25mg once daily. It may be increased at interval of 2 weeks to
maximum dose of 50mg daily.
Cont…
Peripheral Vasodilators
• Relax blood vessels to improve blood flow, thus decreasing blood
pressure.
Hydralazine and Minoxidil.
• Hydralazine decreases systemic resistance through direct vasodilation
of arterioles.
• Minoxidil relaxes arteriolar smooth muscle, causing vasodilation,
which, in turn, may reduce blood pressure.
Cont…
Doses:
• Hydralazine: Orally, 25mg every 12 hours (max. 50mg 12
hourly). IV slow injection 5-10mg over 20 minutes (may be
repeated after 20-30minutes). IV infusion, initially 200-
300μg/minute. Maintenance usually 50-150 μg/minute.
Cont…
Calcium Channel Blockers
• Amlodipine , Nifedipine (Adalat)
Dose:
• Amlodipine 5-10mg once daily,
• Nifedipine 20-40mg twice daily
Cont…
Angiotensin-converting Enzyme (ACE) Inhibitors
• Competitive inhibitors of ACE. Reduces angiotensin II levels, thus
decreasing aldosterone secretion.
• Prevents conversion of angiotensin I to angiotensin II, a potent
vasoconstrictor, resulting in lower aldosterone secretion.
• Examples: Captopril, Enalapril, Lisinopril , Ramipril.
Cont…

Doses:
• Captopril: 12.5-25 mg PO twice a day (in elderly start with
6.25mg). Usual maintenance dose 25mg twice daily; max 50mg
twice daily (rarely 3 times a daily in severe hypertension)
• Enalapril: 2.5-5 mg/d PO (increase as necessary); range is 10-20
mg/d PO (max 40mg a day in severe hypertension).
• Lisinopril: Initially PO 2.5mg daily, maintenance dose 10-20mg
once a day (max. 40mg daily).
Cont…
Angiotensin II Receptor Antagonists
• For patients unable to tolerate ACE inhibitors
Example; Losartan, Valsartan
• Doses: Losartan: initially 50mg (25mg in elderly),
maintenance dose 25-100mg once daily or in 2 divided
doses.
Cont…
Alpha-adrenergic Agonists
Stimulate presynaptic alpha2-adrenergic receptors in the brain
stem, which reduces sympathetic nervous activity.
• Methyldopa (Aldomet)
Patient Education
• Hypertension is a lifelong disorder.
• For optimal control, a long-term commitment to lifestyle
modifications and pharmacological therapy is required.
• Therefore, repeated in-depth patient education and
counseling not only improve compliance with medical
therapy but also reduce cardiovascular risk factors.
Prognosis
• Most individuals diagnosed with hypertension will have increasing
blood pressure as they age.
• Untreated hypertension is notorious for increasing the risk of
mortality and is often described as a silent killer.
• Mild to moderate hypertension, if left untreated, is associated with a
risk of atherosclerotic disease in 30% of people and organ damage in
50% of people after only 8-10 years of onset.
Complications of Hypertension
• Central nervous system - Intracerebral hemorrhage, encephalopathy,
stroke, transient ischemic attack.
• Ophthalmologic - Fundal hemorrhages, exudates, papilledema.
• Cardiac - LVH, congestive heart failure, angina pectoris, myocardial
infarction.
• Vascular - Aortic dissection, diffuse arthrosclerosis.
• Renal - Nephrosclerosis, renal artery stenosis.
Hypertensive Crisis
• Hypertensive crisis rarely occurs and is characterized by
extremely high blood pressure, diastolic pressure usually
exceeding 130 mm Hg, and evidence of potentially life
threatening end organ dysfunction.
Cont…

The clinical conditions associated with hypertensive crisis

include;
• Hypertensive encephalopathy
• Extreme hypertension with acute pulmonary edema
• Extreme hypertension with acute aortic dissection
• Extreme hypertension with intracerebellar hemorrhage
• Extreme hypertension with an acute myocardial infarction
• Malignant hypertension
THANKS FOR LISTENING
Heart failure

INTERNAL MEDICINE
 Objectives
At the end of this session each participant should be able to
• Define Heart failure
• Explain epidemiology of Heart failure
• Describe pathogenesis of Heart failure
• Explain clinical features of Heart failure
• Explain functional classification
• Describe management of Heart failure
• Provide measures to prevent and control of Heart failure
 Heart failure
• Heart failure: Is a complex syndrome caused by structural or
functional cardiac disorder that impairs the ability of the heart to
pump blood and support physiological circulation. Characterized
by shortness of breath, fatigue and Signs of fluid retention.
• Inability of the myocardium to pump blood to meet the metabolic
demands of the body or consistently elevated filling pressures in
the chambers of the heart.
• Heart failure may be either
• compensated (when the patient is stable) or
• decompensated (when the patient suddenly gets worse)
• There are three types of Heart failure;
• Right sided heart failure (RHF)
• Left sided heart failure (LHF)
• Congestive Heart Failure (Bilateral cardiac failure)
Cont…..
Compasated heart failure
• Physiological responses restore Cardiac output
• Patient is stable

Decompasated heart failure

• Physiological responses fail to restore cardiac output.
• The patient presents with symptoms
RIGHT SIDED HEART FAILURE
• Is characterized by reduction in Right ventricular output and an
increase in Right atrial pressure and systemic venous pressure.
Causes of isolated RHF
• Chronic lung disease
• Pulmonary valvular stenosis
LEFT SIDED HEART FAILURE
• Is characterized by reduction in left ventricular output and an increase
in left atrial pressure and pulmonary venous pressure.
• Acute increase in left atrial pressure causes;
-Pulmonary congestion and
-Pulmonary edema
BIVENTRICULAR HEART
FAILURE :
• In biventricular failure, both sides of the heart are affected.
• This may occur because the disease process such as dilated
cardiomyopathy or ischemic heart disease affects both ventricles
OR
• Because disease of the left heart leads to chronic elevation of left
atrial pressure, pulmonary hypertension and right heart failure.
 Causes of Heart failure
Systolic Dysfunction Diastolic Dysfunction
(Inability to expel blood) (Abnormal filling)
• Hypertension • Hypertension
• Idiopathic cardiomyopathy • Fibrosis
(like HIV) • Ischemia
• Valvular disease • Aging process
• Ischemic heart disease • Constrictive pericarditis
• Alcoholic cardiomyopathy (like TB)
• Drug‐associated • Restrictive pericarditis
cardiomyopathy (endomyocardio fibrosis)
• Myocarditis • Hypertrophic
cardiomyopathy
Pathophysiology:
• Decreased cardiac output triggers the baroreceptors in the LV carotid
sinus and aortic arch. This leads to stimulation of the cardio-
respiratory center in the brains. Increase ADH release (causing
peripheral vasoconstriction and increase renal salt and water
absorption) and
• Increased sympathetic stimulation (activating renin-angiotensin-
aldosterone system, promoting more water retention and peripheral
vasoconstriction).
Cont…..
• These leads to:
 LV dilatation and hypertrophy (poor ejection fraction) .
Increased peripheral vascular resistance (high afterload) and
Retention of fluid (high preload)

• Most patients present with left heart failure which can progresses to
right heart failure. The most common cause of right heart failure is left
heart failure but it can also be caused by pulmonary hypertension
(corpulmonale).
 Clinical Features
• Depending on acuteness and severity Signs and symptoms,
include;
• From history the patient may have; Exertion Dyspnea,
Orthopnea, Paroxysmal Nocturnal Dyspnea, Dyspnea at
Rest, edema, Congestive hepatomegaly, anorexia, bloating,
nausea, and constipation.

• On physical examination the patient may have; Edema,

finger clubbing, anxious, malnourished, Tachycardia,
Hepatomegaly, Pallor, Peripheral cyanosis, Pulmonary
rales, Jugular venous distention, positive Hepatojugular
reflux, Hydrothorax (pleural effusion), Ascites,
Cardiomegaly
 Investigations
Diagnosis is based on medical history and symptoms but
imaging and blood tests are also done
• Echocardiogram(ECHO)
• Baseline echocardiogram to evaluate LV/RV function,
valvular function, pericardial disease
• Echocardiogram yearly if possible to monitor cardiac
function
• Electrocardiogram(ECG) - for ischemic disease, arrhythmias
• Full blood picture and HB level - evaluate anemia
• Blood chemistry - renal and liver function, electrolytes,
• Lipid panel - assess for hyperlipidemia
• CXR - usually used to evaluate for pulmonary edema,
cardiomegaly, pleural effusion.
• Pulse oximetry.
 The New York heart association (NYHA)
functional classification
• The New York heart association (NYHA) functional
classification
Class I: no limitation in physical activity. Ordinary physical
activity does not cause Symptoms of HF.
Class II: slight limitation on ordinary physical activity (fatigue,
SOB)
Class III: marked limitation of activity (comfortable at rest but
slight exertion causes symptoms)
Class IV: symptoms occurred at rest
 Framingham Criteria for CCF
Validated CHF with 2 major criteria or 1 major and 2 minor

Major criteria: Minor criteria:

• 1. Paroxysmal nocturnal • 1. Nocturnal cough
dyspnea or orthopnea, • 2. Dyspnea on ordinary exertion
• 2. Weight loss of 4.5 kg in 5 • 3. Pleural effusion
days in response to treatment • 4. Tachycardia (rate of 120 bpm)
• 3. Neck vein distension • 5. Bilateral ankle edema
• 4. Central venous pressure • 6. A decrease in vital capacity by
>16cm of water 1/3rd the maximal value
• 5. Hepatojugular reflux recorded
• 6. Pulmonary rales
• 7. Acute pulmonary edema
• 8. S3 gallop
• 9. Circulation time of 25
seconds
• 10. Radiographic cardiomegaly
Differential Diagnosis of HF
• Anaemia
• Protein loosing enteropathy
• Nephrotic syndrome
• Chronic renal insufficiency
• Pneumonia
• Acute respiratory distress syndrome
• Asthma
• Myocardial infarction or pericardial diseases
• Pulmonary edema
• Pneumothorax
• Pneumocystis carinii pneumonia
• Pulmonary embolism
 Management
• Lifestyle modifications – critically important to maximize
cardiac function and exercise tolerance
• low or no salt diet → to decrease fluid retention
• fluid restriction → usually 1-2 L of total fluid intake daily
• daily weights → monitor for signs of fluid overload and
allows self-adjustment of medications for signs of fluid
overload

• Limit the use of NSAIDs as they can worsen fluid retention

and lead to worsening renal function
 Management of CCF
• Pharmacological Management– Ideally CCF patients should be
managed with a multi-drug regimen consisting of:
• ACE inhibitor or angiotensin receptor blocker
(ARB) - to decrease Ventricular remodeling
• Captopril 12.5 – 25mg PO BD or TDS,
• Lisinopril 10 – 40 mg PO OD
• Diuretic - for symptomatic relief and to decrease fluid
retention e.g. furosemide 20 – 80mg PO OD or BD
• Beta blocker - to decrease myocardial oxygen
demand, decrease LV remodeling
• carvedilol 6.25mg PO BD, up to 25mg PO BD
• atenolol 12.5mg PO OD, up to 100mg PO OD
• propanolol 40mg PO BD, up to 320mg PO BD
• Digoxin for Class II‐III- symptomatic improvement, but
no mortality benefit. Dose 0.125 – 0.25mg PO OD
• NOTE; Due to resource limitations and financial constraints,
not all medications may be possible. At the minimum an ACE
inhibitor and diuretic should be used. But additional drugs will
add further benefit.
 Causes of CHF exacerbation
Decompensating in failure : FAILURE
• F: forgot to take medication, ran out of medication
• A: arrhythmias (especially atrial fibrillation)
• I: ischemia / infarction / infection
• L: lifestyle (reduce salt diet, stop sedentary life style, stop
smoking, stop alcohol, reduce stress)
• U: up‐regulation (increase metabolic demand eg in pregnancy,
thyrotoxicosis, anemia)
• R: renal failure (fluid overload)
• E: embolism (pulmonary embolism) / endocarditis
 Management of Decompensated
Congestive Cardiac Failure (CCF)
• Diuresis (the mainstay of treatment, 1st dose should be given stat)
• Monitor urine output, daily weights (+/‐ Foley catheter if needed)
• Oxygen therapy for 02 sat < 90% on room air
• Treat exacerbating conditions (such as infection, afibrilation)
• Treat reversible causes of cardiomyopathies (anemia and Thyroid)
• Stop the patient's medications that don’t support improvement
• Low sodium diet
• Symptomatic management of pulmonary edema CCF patient:
Use the following mnemonics LNMP (Last Normal Menustral Period)
• Lasix (L): If low urine output, give furosemide 20 , 40 to 80 mg
IV TDS & consider ICU transfer for lasix drip, If MAP<65, consider
ICU transfer for inotropic assisted diuresis w/ dopamine by
protocol captopril at 6.25mg PO BD, increase as tolerated
• Nitrates (N): If BP tolerates, add isosorbide mononitrate
10mg-20mg 12hrly after other agents have been prescribed
• Morphine (M): initially 3‐5mg IV or IM PRN for shortness of
breath
• Position (P): Position the patient in cardiac posture or
cardiac bed of 45 degree.
 Evaluation
• Define Heart failure
• Explain clinical features of Heart failure
• Describe management of Heart failure
• Provide measures to prevent and control
of Heart failure
 References
• Davidson, S, (2014) - Principles and Practice of
Medicine, 22nd Edition, Churchill Livingstone.
• Longmore, M, et al, (1999), Oxford Handbook of
Clinical Medicine, 6th Edition, Oxford
• Swash, M., & Glynn, M. (2007). Hutchinson’s Clinical
Methods: An Integrated Approach to Clinical Practice:
22nd Edition. Philadelphia, PA: Saunders Elsevier
• Trouse, (2000) Short textbook of Medicine University
Press
• MoHCDGEC Standard treatment guidelines & national
essential medicines list tanzania mainland 2017
• MoHCDGEC/ NACTE (2016). Curriculum for
Technician Certificate (NTA Level 5) Curriculum,
Dodoma.
 Initiating a Vision is a Leader’s
responsibility.

Leaders encourage a dream for their

department , team or company .
But the vision must be widely owned , so
that it can grow through the
participation of many hearts and minds.

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