CRITICAL CARE EMERGENCY

MEDICINE PART 2
DR.MASHUK
Brain Abscess 
 Introduction
o Intracranial abscesses are serious and life-threatening infections. They
include brain abscess and subdural or extradural empyema and are
classified according to the anatomical location or the etiologic agent. The
term brain abscess is used to represent all types of intracranial abscesses.
Brain Abscess 
 Aetiology
o Intracranial abscesses can originate from infection of contiguous structures
(eg, otitis media, dental infection, mastoiditis, sinusitis) secondary to
hematogenous spread from a remote site (especially in patients with
cyanotic congenital heart disease), after skull trauma or surgery, and,
rarely, following meningitis.
Brain Abscess 
 Pathophysiology
o Brain abscess is caused by intracranial inflammation with subsequent
abscess formation. In at least 15% of cases, the source of the infection is
unknown (cryptogenic). Infection may enter the intracranial compartment
directly or indirectly via 3 routes.
 A) Contiguous suppurative focus (45-50% of cases)
 B) Trauma (10% of cases)
 C) Hematogenous spread from a distant focus (25% of cases)
Brain Abscess 
 A)Contiguous suppurative focus (45-50% of cases)
 Direct extension may occur through necrotic areas of osteomyelitis in the
posterior wall of the frontal sinus, as well as through the sphenoid and
ethmoid sinuses.This direct route of intracranial extension is more
commonly associated with subacute and chronic otitic infection and
mastoiditis than with sinusitis.Frontal or ethmoid sinus infections generally
spread to the frontal lobes. Odontogenic infections can spread to the
intracranial space via direct extension or a hematogenous route. These
infections also generally spread to the frontal lobe.
Brain Abscess 
 The frequency of brain abscesses resulting from ear infections has declined
in developed countries. However, abscesses complicating sinusitis has not
decreased in frequency.Contiguous spread could extend to various sites in
the central nervous system, causing cavernous sinus thrombosis;
retrograde meningitis; and epidural, subdural, and brain abscess.
 The valveless venous network that interconnects the intracranial venous
system and the vasculature of the sinus mucosa provides an alternative
route of intracranial bacterial entry. Thrombophlebitis originating in the
mucosal veins progressively involves the emissary veins of the skull, the
dural venous sinuses, the subdural veins, and, finally, the cerebral veins.
By this mode, the subdural space may be selectively infected without
contamination of the intermediary structure.
Brain Abscess 
 Intracranial extension of the infection by the venous route is common in
paranasal sinus disease, especially in acute exacerbation of chronic
inflammation. Chronic otitis media and mastoiditis generally spread to the
inferior temporal lobe and cerebellum, causing frontal or ethmoid sinus
infection and dental infection of the frontal lobe.
Brain Abscess 
 B)Trauma (10% of cases)
 Trauma that causes an open skull fracture allows organisms to seed
directly in the brain. Brain abscess can also occur as a complication of
intracranial surgery, and foreign body, such as bullets. Occasionally brain
abscess can develop after trauma to the face.
Brain Abscess 
 C)Hematogenous spread from a distant focus (25% of cases)
 These abscesses are more commonly multiple and multiloculated and are
frequently found in the distribution of the middle cerebral artery. The most
common effected lobes (in descending frequency) are the fontal, temporal,
parietal, cerebellar, and occipital.
 These infections are associated with cyanotic heart disease (mostly in
children), pulmonary arteriovenous malformations, endocarditis, chronic
lung infections (eg, abscess, empyema, bronchiectasis), skin infections,
abdominal and pelvic infections, transplantation, injection drug use, and
HIV infection.
Brain Abscess 
 Clinical Presentation
o Symptoms
 Onset may be sudden or subacute over several weeks.
 Common presenting symptoms include fever, headache, changes in mental
state (drowsiness, confusion), focal neurological deficits, grand mal
seizures, nausea and vomiting, neck stiffness.
 A suddenly worsening headache, followed by emerging signs of
meningism, are often associated with rupture of the abscess.
Brain Abscess 
o Signs
 Fever.
 Focal motor or sensory deficits.
 Raised blood pressure and bradycardia associated with raised intracranial
pressure.
 Papilloedema.
 Ataxia.
 Confusion, drowsiness.
 Bulging fontanelle in infants.
Brain Abscess 
 Physical Findings
 Low-grade or high-grade fever,Persistent headache (often
localized),Drowsiness,Confusion,Stupor,General or focal seizures,Nausea
and vomiting,Focal motor or sensory
impairments,Papilledema,Ataxia,Hemiparesis,Neck stiffness +
 Cerebellar abscess - Nystagmus, ataxia, vomiting, and dysmetria
 Brainstem abscess - Facial weakness, headache, fever, vomiting,
dysphagia, and hemiparesis
 Frontal abscess - Headache, inattention, drowsiness, mental status
deterioration, motor speech disorder, hemiparesis with unilateral motor
signs, and grand mal seizures
 Temporal lobe abscess – Headache and aphasia
 Occipital abscess- Neck rigidity and visual defects
Brain Abscess 
 Differential Diagnosis
o Meningitis.
o Encephalitis.
o Brain tumour or other intracranial space-occupying lesion.
Brain Abscess 
 Investigations
o FBC
o CSF study
o Blood for C/S
o CRP
o RFT
o Sr.Electrolytes
o CT/MRI
o Aspiration of abscess for C/S
o Biopsy for cerebral lesion
Brain Abscess 
 Management
 Drain intracranial collection; supratentorial abscesses can be drained via a
burr hole. Pus should be sent for culture.
 Administer effective antibiotic therapy; early treatment is essential.
 Eliminate the primary source of infection.
Brain Abscess 
 Complications
o Intracerebral abscesses may rupture into the ventricular system and
produce ventriculitis.
o Mainly depending on the speed of diagnosis and treatment, 20-80% of
survivors have neurological sequelae - eg, hemiparesis, visual field loss.
Brain Abscess 
 Prognosis
 Prompt treatment results in mortality of less than 10%, but a delay in
diagnosis increases mortality to above 50%.
 Rupture of a brain abscess is associated with mortality of up to 80%.
 50% of survivors have neurological sequelae which may include
hemiparesis, visual field losses.
Sepsis 
 Introduction
o Sepsis is a serious medical condition caused by an overwhelming immune
response to infection. Chemicals released into the blood to fight infection
trigger widespread inflammation.
o Inflammation may result in organ damage. Blood clotting during sepsis
reduces blood flow to limbs and internal organs, depriving them of
nutrients and oxygen. In severe cases, one or more organs fail. In the worst
cases, infection leads to a life-threatening drop in blood pressure, called
septic shock. This can quickly lead to the failure of several organs -- lungs,
kidneys, and liver -- causing death.
Sepsis 
 Etiology and Pathophysiology
 Sepsis is not a random occurrence and is usually associated with other
conditions, such as perforation or rupture of an intra-abdominal or pelvic
structure. Intrarenal infection (pyelonephritis), renal abscess (intrarenal or
extrarenal), acute prostatitis, or prostatic abscess may cause urosepsis in
immunocompetent hosts.
 Sepsis or septic shock may be associated with the direct introduction of
microbes into the bloodstream via intravenous (IV) infusion (eg, IV line
infections and other device-associated infections). Meningococcemia from
a respiratory source may also result in sepsis, with or without associated
meningitis.
Sepsis 
 Bacteremia due to bacteriuria (urosepsis) may complicate cystitis in
compromised hosts, and sepsis may be caused by overwhelming
pneumococcal infection in patients with impaired or absent splenic
function.
 The pathophysiology of sepsis is complex and results from the effects of
circulating bacterial products, mediated by cytokine release, caused by
sustained bacteremia. Cytokines are responsible for the clinically
observable effects of the bacteremia in the host.Impaired pulmonary,
hepatic, or renal function may result from excessive cytokine release
during the septic process.
Sepsis 
 Cardio-vascular system in sepsis
 Failure of vascular tone
 Vasodilatation due to local metabolites like lactic acid
 Induced NO release
 Loss of reactivity of smooth muscle
 Failure of microcirculation
 AV Shunting
 Capillary leak and intestitial oedema
 Hemoconcentration, sludging, intravascular coagulation, closure of
capillary
 Myocardial depressant factor
Sepsis 
o Absolute and relative hypovolaemia resulting in hypotension
o Warm peripheries in early stages, cold and shut down in late
decompensated stages
o Myocardial depression
Sepsis 
 CNS in sepsis
 Failure of autoregulation, hypoperfusion, impaired oxygenation, metabolic
encephalopathy and effects of endotoxins
o Confusion, restlessness, irritability, stupor, coma, convulsions and death
Sepsis 
 Respiratory system in sepsis
 Protein rich fluid leaking into the intestitium
 Protein rich fluid leaking into the alveoli
 Hypotension

o Tachypnoea
o Hypoxia
o ARDS
Sepsis 
 Renal system in sepsis
 Oliguria leading onto anuria
 Related to hypotension and hypoperfusion
 Stress hormones
Sepsis 
 Splanchnic circulation and the GI tract
 Ischaemic injury of pancreas
 Hypoperfusion
 Ischaemia of the mucosa and villi
 Denudation of the villi 30min. – 60 min
 Trans mucosal necrosis 4 hours
 Transmural necrosis 6 hours
Sepsis 
 Coagulation in sepsis
 Pro-coagulant state
 Disseminated intravascular coagulation /consumptive coagulopathy
Sepsis 
 Metabolism in sepsis
 Glucose metabolism – hypoglycaemia and hyperglycaemia
 Muscle proteolysis
 Hepatic protein synthesis
 Tissue metabolism prodominantly anaerobic in nature, not energy efficient
Sepsis 
 Clinical Presentation
 SIRS – systemic inflammatory response syndrome
o A collection of signs and symptoms in response to a variety of insults
ranging from trauma to infection
 Temperature >38 degrees C or < 36 degrees C, Heart rate > 90/min,
Respiratory rate > 20/min or PaCO2 < 4.3 kPa, WCC > 12,000 or <
4000/cu.mm
Sepsis 
 Investigations
o CBC
o Urine R/M/E and C/S
o Blood for C/S
o ECG/ECHO
o LFT
o RFT
o BT/CT/PT
o Sr.Electrolytes
o ABG
o CT/MRI
Sepsis 
 Management
o Antibiotics
o Haemodynamic management
Sepsis 
 Specific monitoring
 ECG
 BP
 CVP
 PAWP
 Cardiac output
 Urinary flow
 Fluid balance
 Temperature
 O2 saturation
 ABG
 Lung function