Early monitoring of serum electrolytes in traumatic brain injury (TBI) patients offer valuable prognostic information
Editors:
- Dr. Praful B. Godkar (Ph.D)
Eminent Author, Medical Biochemist and Scientist, Technical Education consultant. AGD Biomedicals (Pvt) LTD. - Dr. Gauri Kulkarni MD (Pathology)
Vice President, AGD Biomedicals (Pvt) LTD.
Dyselectrolytemia is commonly observed in patients with traumatic brain injury (TBI)(1). Early electrolyte imbalances indicate initial effects of brain injury, and prompt serum electrolyte assessment provides useful prognostic data(2-9). Alterations in sodium, potassium, chloride, and calcium concentrations are commonly observed among patients affected by traumatic brain injury (TBI)(2-9). Both hypernatremia and hyponatremia have been identified as potential clinical presentations of traumatic brain injury (TBI) (2,3). Elevated chloride levels are linked to lower Glasgow Coma Scale scores, indicating severe neurological impairment(4-6). Serum potassium levels show significant association with subdural hematoma and subarachnoid hemorrhage highlighting their potential as markers for severe brain injury(5,6). Early monitoring of serum electrolytes with a POCT analyzer like AGD EL-120, along with complete hemogram testing via AGD HT-340, and coagulation factor assessment using the AGD C-102 could be life-saving for TBG patients(11).
NOTE: Hypokalemia typically occurs right after TBI and stays elevated for several days(5,6).
Q1. What is the role of catecholamines in hypokalemia?
ANS: Catecholamines – including epinephrine, norepinephrine, and dopamine—are produced in the adrenal medulla and nervous system. They trigger the “fight-or-flight” response by raising heart rate, blood pressure, and respiration. Hypokalemia is predominantly attributed to catecholamine-mediated shifts in potassium, occurring in a range of clinical scenarios including stress, significant fluid loss, renal potassium depletion, and hypothermia(11).
Q2. What biochemical changes related to serum potassium occur following the release of catecholamines?
ANS: Catecholamines play a vital role in the regulation of rapid, transcellular potassium transfer. When they act on adrenergic receptors, the extracellular fluid enters into the cells, primarily in skeletal muscle. This action triggers acute hypokalemia in high-stress situations(11).
Q3. What is Glasgow Coma Scale (GCS)?
ANS: The Glasgow Coma Scale (GCS) is recognized internationally as the standard tool for evaluating a patient’s level of consciousness following brain injury or medical emergency.
Q4. What is the significance of GCS?
ANS: The primary function of the GCS is to provide healthcare professionals with an objective and standardized framework for accurately conveying the neurological status of critically ill patients. GCS categorizes brain injuries into three levels: Mild (13–15), Moderate (9–12), and Severe (3–8). Typically, a score of 8 or below signals a coma, suggesting the patient might not be able to maintain their airway and may need intubation.
CASE STUDY
A middle-aged male patient was admitted to a tertiary care center, following severe head injury. His blood test reports were as follows:
COMPLETE HEMOGRAM
| PARAMETER | RESULT | REFERENCE |
| Hemoglobin | 10.7 g/dl | 13–18 g/dl |
| Total erythrocyte count | 4.25 X 1012 /l | 5.0 ± 0.5 X 1012 /l |
| Total leukocyte count | 14.5 X 109/l | 7.0 ± 3.0 X 109/l |
| Differential leukocyte count | ||
| Neutrophils | 82% | 40–75% |
| Lymphocytes | 17% | 20–45 % |
| Monocytes | 1% | 2–8 % |
| PCV | 30% | 36–48% |
| MCV | 82 fL | 82–92 fL |
| MCH | 29 pg | 27–32 pg |
| MCHC | 33 % | 32–36 % |
| RDW- CV | 14 | 12–14 |
| Platelet count | 275 X 109/l | 150–400 X 109/l |
| MPV | 10.5 fL | 7.5-12 fL |
| PDW | 16.0 | 15-17 |
| Absolute Neutrophil count | 11,890 | 2,500-7,000 |
| Absolute Lymphocyte count | 2,465 | 1,000-4,000 |
| Absolute monocyte count | 145 | 200-800 |
| Neutrophil/Lymphocyte ratio | 4.5 | 0.78-3.53 |
| Platelet/Lymphocyte ratio | 99.39 | 97-194 |
| Systemic immune-inflammatory Index | 1116 | > 500 |
| Metzer Index (MI) | 19.2 | > 13 |
STAINED BLOOD SMEAR EXAMINATION OBSERVATIONS:
Morphology of Red blood cells: Normal cells
Morphology of White blood cells: Normal morphology and Increased number of WBCs with predominating Neutrophils.
INTERPRETATION OF COMPLETE HEMOGRAM
(A) Significant blood loss from traumatic brain injury (TBI) can lead to low hemoglobin levels and normochromic normocytic anemia.
(B) An elevated white blood cell (WBC) count, or leukocytosis, is a standard physiological response to trauma. It serves as a primary indicator of Systemic Inflammatory Response Syndrome (SIRS), as indicated by high SII value in this case.
(C) A marked rise in the Neutrophil/Lymphocyte ratio and Platelet/Lymphocyte ratio suggests advancing inflammation in the body of the patient.
Q5. What are SIRS and SII?
ANS: SIRS (Systemic Inflammatory Response Syndrome) is a serious inflammatory disorder that can result from trauma, infection, surgery,etc. SII stands for Systemic Inflammatory Index. It is calculated from CBC report as follows: Platelet count X Neutrophil count/Lymphocyte count.
Q6. What is the clinical significance of SII?
ANS: SII has been used as a marker of subclinical inflammation and prognosis. It could be used to predicts rapid progression to sepsis, organ dysfunction, and increased mortality.
NOTE : A hematology analyzer quickly provides NLR, PLR, and SII from a CBC test in 2–3 minutes.
SERUM ELECTROLYTES
| PARAMETER | RESULT | REFERENCE |
| Serum Sodium | 154 mEq/l | 133–146 mEq/l |
| Serum Potassium | 2.8 mEq/l | 3.8–5.6 mEq/l |
| Serum Chlorides | 109 mEq/l | 95–106 mEq/l |
INTERPRETATION
Increased serum sodium and chlorides and decreased serum potassium indicate Dyselectrolytemia, which is commonly observed in patients with traumatic brain injury (TBI)(1-10).
COAGULATION PANEL TESTS
| PARAMETER | RESULT | REFERENCE |
| Prothrombin time (PT) | 21 seconds | 12–16 seconds |
| Activated partial thromboplastin time: (APTT) | 44 seconds | 35–40 seconds |
| Thrombin time (TT) | 25 seconds | 15–20 seconds |
INTERPRETATION
A high TT, along with high PT and aPTT, provides strong evidence of a defect with the final stages of coagulation that increases the risk of bleeding(9).
References
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- Kolmodin, L.; Sekhon, M.S.; Henderson, W.R.; Turgeon, A.F.; Griesdale, D.E. Hypernatremia in Patients with Severe Traumatic Brain Injury: A Systematic Review. Ann. Intensive Care 2013, 3, 35.
- Petra, C.M.D.-G.; Jean-Michel, M.; Maurice, D.; Eric, G.; Peter, C.R. Acute Symptomatic Hyponatremia and Cerebral Salt Wasting after Head Injury: An Important Clinical Entity. J. Pediatr. Surg. 2001, 36, 1094–1097.
- Xiaofeng, M.; Baozhong, S. Traumatic Brain Injury Patients with a Glasgow Coma Scale Score of ≤8, Cerebral Edema, and/or a Basal Skull Fracture Are More Susceptible to Developing Hyponatremia. J. Neurosurg. Anesthesiol. 2016, 28, 21.
- Schaefer, M.; Link, J.; Hannemann, L.; Rudolph, K. Excessive Hypokalemia and Hyperkalemia Following Head Injury. Intensive Care Med. 1995, 21, 235–237.
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- Emily, J.M.; Stubna, M.D.; Holena, D.; Reilly, P.; Seamon, M.; Brian, P.S.; Kaplan, L.; Jeremy, W.C. Abnormal Calcium Levels During Trauma Resuscitation Are Associated with Increased Mortality, Increased Blood Product Use, and Greater Hospital Resource Consumption: A Pilot Investigation. Anesth. Analg. 2017, 125, 895.
- Rodríguez-Triviño, C.Y.; Torres Castro, I.; Dueñas, Z. Hypochloremia in Patients with Severe Traumatic Brain Injury: A Possible Risk Factor for Increased Mortality. World Neurosurg. 2019, 124, e783–e788.
Lee, J.Y.; Hong, T.H.; Lee, K.W.; Jung, M.J.; Lee, J.G.; Lee, S.H. Hyperchloremia is Associated with 30-Day Mortality in Major Trauma Patients: A Retrospective Observational Study. Scand. J. Trauma Resusc. Emerg. Med. 2016, 24, 117.
Jahanipour, A.; Asadabadi, L.; Torabi, M.; Mirzaee, M.; Jafari, E. The Correlation of Serum Chloride Level and Hospital Mortality in Multiple Trauma Patients. Adv. J. Emerg. Med. 2020, 4, e4.
Godkar PB, Godkar DP. Textbook of Medical laboratory technology (4th edition, 2024), Bhalani Publishers, Mumbai. India.
