ISSN:(O) 2320-5407, ISSN(P) 3107-4928 Int. J. Adv. Res.

13(10), October-2025, 1512-1519

Journal Homepage: -www.journalijar.com

Article DOI:10.21474/IJAR01/22051
DOI URL: http://dx.doi.org/10.21474/IJAR01/22051

RESEARCH ARTICLE

INCIDENCE OF HYPOPHOSPHATEMIA IN PATIENTS WITH SEVERE

TRAUMATIC BRAIN INJURY AND ITS IMPACT ON MORTALITY: A
RETROSPECTIVE STUDY
Mohammed Rabi Andaloussi1,2, Rida Touab1, Khalil Mounir1, Abdelhamid Jaafari1, Mustapha Bensghir1 and
Hicham Balkhi1

1. Department of Anesthesiology and Intensive Care– Military Teaching Hospital Mohammed V- Rabat-Morocco.
2. Faculty of Medicine and Pharmacy of Casablanca- HASSAN II University of Casablanca- Morocco.
……………………………………………………………………………………………………....
Manuscript Info Abstract
……………………. ………………………………………………………………
Manuscript History Background: Hypophosphatemia is a common electrolyte disturbance
Received: 19 August 2025 in critically ill patients, particularly those with severe traumatic brain in
Final Accepted: 21 September 2025 jury(TBI).Phosphate plays essential roles in bone structure, cellular ene
Published: October 2025 rgy metabolism, membrane integrity, and acid-base balance. Despite its
clinical relevance, data on the incidence, risk factors, and consequences
Key words:-
Hypophosphatemia; Traumatic brain of hypophosphatemia in TBI patients remain limited.
injury; Neurocritical care; Methods: We conducted a retrospective observational study of patients
with severe TBI admitted to a surgical intensive care unit (ICU). Serum
phosphate levels were measured at ICU admission and at 72 hours. We
evaluated the incidence of hypophosphatemia, its potential causes and
its clinical consequences.
Results: Among 106 patients with severe TBI, hypophosphatemia
occurred in 55.6% at ICU admission and persisted in 49% at 72 hours.
Risk factors included insulin therapy,respiratory alkalosis, catecholami
ne administration, higher mannitol use, and greater illness severity.
Hypophosphatemia was associated with longer mechanical ventilation,
higher incidence of arrhythmias, and increased nosocomial infections.
Importantly, hypophosphatemia remained an independent predictor of
28 day mortality after adjustment for confounding variables.
Conclusions: Hypophosphatemia is frequent and clinically significant
in patients with severeTBI, contributing to multiple systemic complicati
ons and worse outcomes. Routine monitoring of serum phosphate and
targeted supplementation,particularly in severe cases, may be warranted
Further prospective studies are needed to determine whether correcting
moderate hypophosphatemia improves prognosis in this population.

"© 2025 by the Author(s).Published by IJAR under CC BY 4.0. Unrestricted use allowed
with credit to the author."
……………………………………………………………………………………………………....
Introduction:-
Phosphorus, the principal intracellular anion, is essential for all living organisms and plays a critical role in
maintaining both the structural and functional integrity of cells. It is a major constituent of the phospholipid bilayer

Corresponding Author:-Mohammed Rabi Andaloussi 1512

Address:-1. Department of Anesthesiology and Intensive Care Military Teaching Hospital Mohammed
V- Rabat-Morocco.2. Faculty of Medicine and Pharmacy of Casablanca- HASSAN II University of
Casablanca, Morocco.
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of cell membranes and participates in numerous biological processes, including adenosine triphosphate (ATP)
production, glycolysis, pH buffering, 2,3-diphosphoglycerate (2,3-DPG) synthesis, mitochondrial function,
enzymatic regulation, signal transduction, and nucleotide metabolism [1–3].Phosphorus also serves as a substrate for
ATP generation, which is crucial for normal neurological function and muscle contraction. Therefore, maintaining
normal serum phosphate levels is of paramount importance. Despite its physiological significance, serum phosphate
remains a neglected parameter in clinical practice.Due to limited awareness regarding hypophosphatemia, practices
surrounding its diagnosis and management vary widely. Some units do not routinely monitor phosphate level, while
others administer supplementation prophylactically, such as before initiating parenteral nutrition or mechanical
ventilation.Hypophosphatemia can have significant clinical consequences, particularly in the intensive care setting.
It impairs cellular energy metabolism and is associated with reduced cardiac and diaphragmatic contractility[4-6]. In
sepsis, hypophosphatemia occurs in up to 60% of cases and may contribute to leukocyte dysfunction [7,8].

Normal plasma phosphate levels range from 0.80 to 1.60 mmol/L. Hypophosphatemia is reported in 2–3% of
hospitalized patients; however, this likely underestimates its true prevalence due to the lack of routine phosphate
monitoring. In patients with traumatic brain injury (TBI), the prevalence can be as high as 50% [9].Severe
hypophosphatemia defined as serum phosphate < 0.3 mmol/L.Several factors contribute to hypophosphatemia in
neurocritical care, including malnutrition, gastric aspiration, liver failure, sepsis, chronic alcoholism, respiratory
alkalosis, volume expansion, glucose infusions, hemodialysis, administration of mannitol, antacids, catecholamines,
and sodium bicarbonate.Unlike other electrolyte disturbances, such as dysnatremia or dyskalemia, phosphate
disturbances are often overlooked in TBI management. Hypophosphatemia frequently goes undiagnosed, as it is
asymptomatic or manifests with non-specific symptoms, including fatigue or irritability. It has been associated with
prolonged ICU and hospital stays. However, whether hypophosphatemia directly affects mortality in neurosurgical
ICU patients remains controversial.Although several studies have linked hypophosphatemia in the ICU to increased
mortality, it remains unclear whether it is a causative factor or simply a marker of illness severity. Data evaluating
the impact of phosphate levels at ICU admission on outcomes in patients with severe traumatic brain injury (TBI)
are limited. We hypothesized that hypophosphatemia negatively influences 28-day mortality in neurocritical care
patients. To investigate this, we performed a retrospective, single-center cohort study comparing 28-day mortality
between patients with hypophosphatemia and those with normal phosphate levels. The primary outcome was 28-day
mortality.

Patients and Methods:-

Study Population:
This was an observational retrospective study conducted from January 1, 2015, to December 31, 2018, in the
Surgical Intensive Care Unit (ICU) of Military Teaching Hospital, Mohammed V Rabat, Morocco.

Inclusion criteriawere:
1. Isolated TBI (Glasgow Coma Scale < 12)
2. Age ≥16 years
3. Availability of serum phosphate measurement at ICU admission and at 72 hours
4. the 28-day follow-up

Exclusion criteriawere:
1. Age <16 years
2. Pregnancy
3. Loss to follow-up
4. Absence of phosphate measurement at ICU admission

During the study period, 1,569 patients were admitted, of whom 143 had TBI. After applying exclusion criteria, 37
patients were excluded, yielding a final cohort of 106 patients.

Clinical and Biological Data Collection:

Patient data were extracted from medical records. Collected variables included:Demographics and baseline
characteristics: age, sex, initial GCS, mechanism of injury, medical history, nutritional status, APACHE II score.
Biological parameters: serum phosphate at admission and 72 h, serum potassium, sodium, calcium, creatinine,
arterial pH, pCO₂, bicarbonate, and urine output prior to admission.Therapeutic interventions: fluid resuscitation,
corticosteroids, catecholamines, insulin therapy, mannitol administration, therapeutic hypothermia, mechanical

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ventilation, and tracheostomy.Outcomes: occurrence of seizures, arrhythmia, nosocomial infection, duration of

mechanical ventilation, ICU length of stay, hospital length of stay, and 28-day mortality.

Statistical Analysis:
Statistical analyses were performed using SPSS version 20.0 .Continuous variables were expressed as mean ±
standard deviation (SD) or median with interquartile range (IQR), and categorical variables as counts and
percentages.Comparisons between groups were performed using the Student’s t-test or Mann–Whitney U test for
continuous variables and Chi-square test for categorical variables.Univariate analysis assessed associations between
clinical/biological variables and 28-day mortality. Variables with p < 0.05 were included in a multivariate logistic
regression model to identify independent predictors, with calculation of odds ratios (OR) and 95% confidence
intervals (CI). Ap-value< 0.05 was considered statistically significant.

Results:-
Patient Characteristics:
Among 1,569 ICU admissions, 106 patients met inclusion criteria. Of these, 59 (55.6%) had hypophosphatemia , 35
(33%) had normal phosphate levels and 12(11,3%) had Hyperphosphatemia. Patient characteristics are summarized
in Table 1.

The mean age was 44.2 ± 8.4 years, and 72.3% were male, with no significant differences between groups. The
mean APACHE II score was 21.2 ± 5.8. Overall 28-day mortality was 37%. Road traffic accidents accounted for
82% of injuries. The mean initial GCS was 7.9 ± 1.5.Diabetes mellitus and chronic alcohol use were significantly
more frequent in the hypophosphatemia group, while hypertension and chronic kidney disease prevalence were
similar between groups.Pre-ICU admission urine output was higher in hypophosphatemic patients (mean 1,430 ±
185 mL). Nutritional support was primarily enteral (85%), with exclusive parenteral nutrition in 3% and combined
enteral–parenteral in 11.7%.

Incidence of Hypophosphatemia:
Median serum phosphate at admission was 0.68 mmol/L (IQR 0.47–1.08). Hypophosphatemia occurred in 59/106
patients (55.6%), including eight with severe hypophosphatemia (<0.3 mmol/L).At 72 hours, 12
normophosphatemic patients developed phosphate <0.6 mmol/L, while 19 hypophosphatemic patients normalized
(>0.8 mmol/L). Overall, hypophosphatemia incidence declined from 55.6% to 49%, with median phosphate rising to
0.72 mmol/L. (Cohort : 94 patients + 12 patients with Hyperphosphatemia on admission).

Biological Parameters:
Serum potassium and arterial pCO₂ were lower in hypophosphatemic patients. Median arterial pH was 7.47 vs. 7.38
in controls. Serum bicarbonate, creatinine, and calcium did not differ significantly.

Therapeutic Interventions:
Hypophosphatemic patients received larger pre-ICU admission fluid volumes (1,500 ± 200 mL vs. 850 ± 150 mL, p
= 0.01) and more mannitol (240 ± 44 mL). Short-term corticosteroids were used in 35% vs. 20% (p = 0.01).
Catecholamine support was required in 40%, and insulin therapy in 72%. Therapeutic hypothermia was applied in
9.5%. Eighty-eight patients were intubated, and 50 underwent tracheostomy for prolonged ventilation.

Variables Total (n=94) Normophosphatemia Hypophosphatemia p-value

(n=35) (n=59)
Clinicalcharacteristics
Age (years) mean ± SD 44.15 ± 18.38 44.87 ± 8.12 44.35 ± 8.7 0.32
Male sex, n (%) 68 (72.3%) 24 (68%) 44 (74.5%) 0.21
GCS score (mean ± SD) 7.9 ± 1.5 8.24 ± 1.3 7.83 ± 1.16 0.08
Mechanism of traumatic brain injury
(%)
Road traffic accident 78 (82%) 28 (80%) 50 (84%) 0.08
Work-related accident 3 (3.1%) 2 (5%) 1 (1.6%) 0.02
Domestic accident 6 (6.3%) 2 (5%) 4 (6.7%) 0.12
Other 7 (7.4%) 3 (8.5%) 4 (6.7%) 0.07

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Medicalhistory
Diabetesmellitus, n (%) 22 (23%) 5 (14.2%) 17 (28%) 0.002
Hypertension (HTN), n (%) 9 (9.5%) 4 (11%) 5 (8%) 0.18
Kidneydisease, n (%) 3 (3%) 1 (2.8%) 2 (3%) 0.23
Alcoholism, n (%) 27 (28.7%) 5 (14.2%) 22 (37.2%) 0.001
Nutrition (%)
Enteral nutrition 80 (85%) 30 (85%) 50 (84.7%) 0.32
Parenteral nutrition 3 (3%) 1 (2.8%) 2 (3%) 0.44
Mixed nutrition 11 (11.7%) 4 (11.4%) 7 (11.8%) 0.27
APACHE II score (mean ± SD) 21.2 ± 5.8 13.7 ± 4.9 26.3 ± 4.7 0.01
Diuresis (ml) mean ± SD 1150 ± 130 713 ± 95 1430 ± 185 0.01
Biologicalparameters
Phosphate at admission (mmol/L) median 0.68 [0.47, 1.12 [0.90, 1.25] 0.48 [0.34, 0.59] 0.01
[IQR] 1.08]
Phosphate at 72h (mmol/L) median [IQR] 0.72 [0.53, 1.20 [0.98, 1.30] 0.54 [0.43, 0.68] 0.01
1.15]
Potassium (mmol/L) median [IQR] 3.6 [3.3, 4.2] 3.9 [3.6, 4.4] 3.4 [3.2, 3.8] 0.01
Creatinine (µmol/L) median [IQR] 81 [65, 108] 78 [52, 95] 83 [68, 112] 0.25
Calcium (mmol/L) median [IQR] 1.91 [1.72, 1.98 [1.76, 2.02] 1.92 [1.77, 2.08] 0.62
2.04]
pH (median [IQR]) 7.42 [7.38, 7.38 [7.34, 7.42] 7.47 [7.42, 7.50] 0.01
7.45]
pCO2 (mmHg) median [IQR] 34 [32, 38] 38 [35, 40] 32 [30, 35] 0.01
HCO3- (mmol/L) median [IQR] 21 [18, 25] 20 [17, 24] 22 [18, 26] 0.32
Therapeutic interventions
Fluid resuscitation (ml) mean ± SD 1280 ± 180 850 ± 150 1500 ± 200 0.01
Corticosteroids, n (%) 28 (30%) 7 (20%) 21 (35%) 0.01
Mannitol (ml) mean ± SD 210 ± 40 162 ± 35 240 ± 44 0.01
Insulintherapy, n (%) 68 (72%) 22 (63%) 46 (77%) 0.01
Hypothermia, n (%) 7 (7.5%) 3 (8.5%) 4 (6.7%) 0.25
Catecholamines, n (%) 38 (40%) 12 (34%) 26 (44%) 0.01
Mechanical ventilation, n (%) 88 (93.6%) 33 (94%) 55 (93%) 0.65
Tracheostomy, n (%) 50 (53%) 18 (51%) 32 (54%) 0.18

Table1: Clinical Characteristics, Biological Parameters and therapeutic interventions of the Study Population

Outcomes:
28-day mortality was higher in hypophosphatemic patients (40% vs. 31%, p = 0.01). Median ICU stay was longer
(17 vs. 10 days, p = 0.01), as was total hospital stay. Duration of mechanical ventilation was also increased (median
14 days). Seizure incidence was 24%, with no difference between groups. (Table2)

Total Normo- Hypophosphatemia p

(n = 94) phosphatemia (n = 59) value
(n = 35)
Seizures, n (%) 23 (24%) 9 (25%) 14 (23.7%) 0.28
Arythmia,n (%) 36 (38%) 12 (34%) 24 (40%) 0.03
Nosocomial infections, n (%) 58 (61%) 19 (54%) 39 (66%) 0.04
Duration of mechanical ventilation, days 10 (4–14) 7 (3–10) 14 (5–17) 0.01
(median [IQR])
ICU length of stay, days (median [IQR]) 14 (6–19) 10 (5–13) 17 (8–21) 0.01
Hospital length of stay, days (median [IQR]) 37 (27– 31 (24–38) 42 (32–47) 0.01
43)

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28-day mortality, n (%) 35 (37%) 11 (31%) 24 (40%) 0.01

Table 2: Clinical outcomes according to serum phosphate status

Predictive factors of 28-day mortality:-

Univariate analysis demonstrated that APACHE II score, hypocapnia, cardiac arrhythmias, and hypophosphatemia
were significantly associated with 28-day mortality. Age, sex, hypokalemia, and nosocomial infection did not reach
statistical significance.Multivariate logistic regression revealed that hypophosphatemia remained an independent
predictor of 28-day mortality (OR 1.75, 95% CI 1.15–2.10, p = 0.01), along with APACHE II score. The other
variables lost their independent predictive value. (Table 3)

Associatedfactors Univariateanalysis Multivariateanalysis

OR 95% CI p-value Adjusted OR 95% CI p-value
Age 1.52 (0.58, 2.3) 0.45 – – –
Male sex 0.80 (0.6, 3.5) 0.63 – – –
APACHE II 1.5 (1.35, 1.6) 0.01 1.45 (1.28, 1.51) 0.01
Hypocapnia 1.21 (1.15, 1.35) 0.02 1.3 (0.86, 2.3) 0.56
Hypokalemia 0.84 (0.35, 2.05) 0.72 – – –
Hypophosphatemia 1.85 (1.25, 2.4) 0.01 1.75 (1.15, 2.1) 0.01
Cardiacarrhythmia 1.12 (1.05, 1.35) 0.04 1.06 (0.75, 1.25) 0.47
Nosocomial infection 1.6 (0.8, 3.5) 0.85 – – –
Table 3: Predictive factors of 28-day mortality.

Discussion:-
Phosphorus is essential for life, present in all organisms, and abundant in the diet (e.g., meat, fish, dairy, nuts, soy).
It is a key component of numerous biomolecules, fulfilling both structural and functional roles.Approximately 85%
of total body phosphorus (~600 g in adults) is stored in bone, serving as the primary phosphate reservoir.
Phosphorus is mobilized to the bloodstream or incorporated into bone tissue according to metabolic and hormonal
demands.Phosphorus is a major constituent of biological membranes, primarily as phospholipids forming bilayers
with embedded proteins. Cellular membranes contain ~40% lipids, predominantly phospholipids. It participates in
intracellular signaling, enzyme regulation, and metabolic pathways such as glycolysis and cholesterol synthesis,
which rely on phosphorylated intermediates. Serum phosphate depletion reduces 2,3-BPG levels, impairing tissue
oxygen delivery [10].Phosphate acts as an effective urinary buffer (pKa 6.8) and contributes to urinary pH
regulation, though its buffering capacity in blood is relatively modest [11].It is important to note that
hypophosphatemia does not necessarily indicate phosphorus depletion. Hypophosphatemia may occur in the
presence of low, normal, or even elevated total body phosphorus levels.

In the latter two cases, a shift of phosphate from the extracellular to the intracellular compartment is observed.
Conversely, phosphorus depletion may exist despite normal, low, or high serum phosphate levels.Phosphorus
depletion corresponds to a reduction in total body phosphorus content.The normal plasma phosphate concentration
ranges from 0.80 to 1.60 mmol/L. Hypophosphatemia can be arbitrarily divided into moderate (plasma phosphate
0.32–0.60 mmol/L) and severe forms (plasma phosphate <0.32 mmol/L).The reported incidence of
hypophosphatemia varies from 0.2% to 2.2% among all hospitalized patients, but may reach 21.5% or higher in
certain patient series. During hospitalization, its incidence tends to increase; thus, a single measurement likely
underestimates the true occurrence of hypophosphatemia.

We conducted an observational study of a specific cohort of patients with traumatic brain injury (TBI) admitted to
asurgical intensive care unit, in order to investigate the incidence of hypophosphatemia and its relationship with
mortality.We reported an incidence of 55.6% in our population.Previous studies have demonstrated that the
incidence of hypophosphatemia varies widely depending on hospital settings andclinical conditions (Table
4).Hypophosphatemia is particularly frequent in cases of sepsis (80%) [7], brain death (72%) [12], and may reach
100% in patients with severe burns, as reported in a 1997 study [13].To our knowledge, only one previous study,
conducted in 2000, focused specifically on patients with traumatic brain injury. That study included 18 patients and
reported an incidence of 61% [19], which is relatively close to the incidence observed in our cohort (55.6%).

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(Table 4)
Author Year Study population / Clinical Number Definition of Prevalence Incidence
setting of hypophosphatemia
patients
Goldstein et 1985 Thoracicsurgery 34 < 0.80 mmol/L – 56%
al [16] Cardiacsurgery 40 50%
Zazzoet al 1995 Surgical ICU 208 < 0.80 mmol/L – 28.8%
[15] < 0.50 mmol/L 17.9%
< 0.20 mmol/L 2.4%
Buellet al 1998 Hepaticsurgery 35 < 0.80 mmol/L – 67%
[20]
Cohen et al 2004 Cardiacsurgery 566 < 0.48 mmol/L – 34.3%
[14]
Salem et al 2005 Hepaticsurgery 20 < 0.70 mmol/L – 100%
[17]
Daily et al 1990 Trauma patients 12 < 0.80 mmol/L – 75%
[18] < 0.50 mmol/L 56%
Kruseet al 1992 Mixed ICU 418 < 0.80 mmol/L – 28%
[21]
Mariket al 1996 Refeeding after >48 h of 62 < 0.65 mmol/L – 34%
[22] fasting < 0.32 mmol/L 6%
Berger et al 1997 Burn patients 16 < 0.80 mmol/L – 100%
[13] < 0.30 mmol/L 50%
Barak et al 1998 Sepsis 99 < 0.80 mmol/L 80% –
[7] Infection without sepsis 32 65%
Sepsis with negative blood 37 80%
cultures
Sepsis with positive blood 30 80%
cultures
Poldermanet 2000 TBI 18 < 0.60 mmol/L 61% –
al [19]
Milioniset al 2002 Intensive cardiac care unit 86 < 0.77 mmol/L 13% –
[23]
Domínguez- 2005 Brain-dead patients 50 < 0.80 mmol/L 72%
Roldánet al
[12]
Present 2019 TBI 106 < 0.80 mmol/L 55.6%
study < 0.30 mmol/L 7.5%
(Andaloussie
t al, 2019)
Table 4: Prevalence and incidence of hypophosphatemia.

Our findings clearly demonstrate that patients with severe traumatic brain injury are at high risk of developing
hypophosphatemia. This observation supports routine measurement of serum phosphate levels upon ICU admission
in this population.Since2012, our unit has implemented systematic phosphate assessment at admission and again at
72 hours of hospitalization. Our results showed that the incidence of hypophosphatemia at 72 hours decreased
slightly to 49%, indicating that this disturbance remains frequent even after initial stabilization. This practice
remains clinically relevant, as it helps identify patients who require closer monitoring to prevent the development of
severe hypophosphatemia, a condition that may necessitate phosphate supplementation before initiating other
intensive interventions such as nutritional support or prolonged mechanical ventilation.The 72-hour measurement
also helps identify patients in whom phosphate levels normalize spontaneously—mainly those with redistribution
hypophosphatemia—and who therefore do not require exogenous supplementation beyond that provided by
nutritional intake.Hypophosphatemia arises via three principal mechanisms: decreased intestinal absorption,
intracellular redistribution, and increased urinary losses.Dietary deficiency is rare due to ubiquitous phosphorus
intake. Prolonged malnutrition or impaired intestinal absorption (e.g., chronic antacid use) may cause depletion

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[24].Vitamin D deficiency reduces intestinal absorption and increases renal phosphate excretion, making
hypophosphatemia an early marker of deficiency [25].Most cases of acute hypophosphatemia result from shifts into
cells, often triggered by intravenous glucose and insulin administration. Refeeding syndrome in malnourished
patients and insulin therapy for diabetic ketoacidosis also cause intracellular phosphate uptake [26].In our cohort,
diabetic patients and those receiving insulin were more common in the hypophosphatemic group (28% vs. 14.2%,
p=0.02; 77% vs. 63%, p=0.01, respectively). Respiratory alkalosis due to hyperventilation, common in agitated or
intubated TBI patients, promotes phosphate influx into cells. Hypocapnia (PaCO₂ 32 vs. 38 mmHg, p=0.01) and
elevated pH (7.47 vs. 7.38, p=0.01) were associated with hypophosphatemia. Renal phosphate wasting is a frequent
contributor, particularly in TBI patients with polyuria from mannitol therapy or central diabetes insipidus. In our
cohort, hypophosphatemic patients received higher mannitol volumes (240 vs. 162 mL, p=0.01) and exhibited
higher urine output (1430 vs. 713 mL, p=0.01). Increased crystalloid administration and corticosteroid use may have
contributed but were unlikely primary drivers.

Although previous studies have linked hypophosphatemia to poor outcomes in critically ill patients [27,28], few
studies have examined the relationship between admission phosphate levels and outcomes in general ICU
populations, and none, to our knowledge, have focused on patients with traumatic brain injury. In our observational
study of traumatic brain injury patients, hypophosphatemia was associated with higher mortality. After adjusting for
the confounding factors, hypophosphatemia remained more frequent among non-survivors. Hypophosphatemic
patients were also more severely ill, but after adjusting for other risk factors, hypophosphatemia remained an
independent predictor of mortality.Some studies support an association between hypophosphatemia and increased
mortality. Zazzo et al. [15] prospectively studied 208 surgical ICU patients, defining hypophosphatemia as <0.8
mmol/L, with a prevalence of 28.8% and higher mortality among hypophosphatemic patients (30% vs. 15.2%; p<
0.05). Sankaran et al. [29] studied 302 ICU patients with bacterial pneumonia, defining hypophosphatemia as <0.77
mmol/L, and found it in 44.7% of patients, who had higher mortality (31.9% vs. 13.2%; p < 0.001).

However, these studies were small, used different definitions of hypophosphatemia, and did not evaluate the
independent relationship between phosphate levels and outcomes after adjusting for disease severity. Only Suzuki et
al. [28] andDemirjian et al. [30] assessed the independent association between hypophosphatemia and mortality,
finding no significant association after adjustment.In 2019, Wang et al. demonstrated in a heterogeneous cohort of
946 ICU patients that admission hypophosphatemia was an independent predictor of 28-day mortality [31]. Our
study confirms these findings and is the first to examine the independent association between hypophosphatemia and
mortality in patients with traumatic brain injury.Our study has several limitations: its retrospective, single-center
design limits generalizability. Only two phosphate measurements were available, restricting assessment of dynamic
changes. Urinary phosphate excretion and kinetic analysis were not performed.

Conclusion:-
Hypophosphatemia in critically ill patients, particularly those with TBI, is common and may contribute to cardiac,
respiratory, neuromuscular, hematologic, and immunologic complications. It can be asymptomatic but also life-
threatening, and is independently associated with increased 28-mortality in this population.Serum phosphate should
be routinely monitored in severe TBI patients, and supplementation considered for symptomatic patients or when
levels fall below 0.32 mmol/L. Whether correcting moderate hypophosphatemia improves outcomes in TBI remains
uncertain and warrants prospective trials. Multicenter studies are needed to clarify optimal phosphate management
strategies in this population.

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