Electrolyte disorders in head injury

1. Electrolyte disorders in head injury
Dr Divakar Goyal
Moderator: Dr Madhur Uniyal

2. 13 year old boy
Mechanism : Fall from Tree
Injury : Multiple abrasions , B/L both bone fracture
Signs and Symptoms : Grade 4 shock , FAST positive in hepaotrenal pouch , Chest
compression test (CCT ) & Pelvic compression test (PCT )- Negative
Treatment :IV Fluids , antibiotics and antiepileptics . Massive blood transfusion .
NCCT Head : Rt frontal contusion with SDH and SAH with no midline shift.

3. • Serial KFT was done
• Urine output 100-120 ml / hr
PID 3 PID4 PID5 PID10
Urea 90 70 56 28
Creatinine 1.1 0.76 0.53 0.42
Sodium 146 154 159 145
Potassium 4.1 3.5 3.23 4.6

4. • What is your diagnosis ?
• What are other investigation we need to do ?
• What are the causes ?
• What is the management ?

5. Electrolyte disorders in Traumatic Brain Injury
One of the preventable secondary brain injuries. Incidence – 59.3%
Risk of development
• Severity of head injury
• Underlying disease-renal failure, cirrhosis, CHF
• Age
• Primary therapeutic strategy -resuscitation fluid, mannitol or diuretics, and
hyperventilation
Van Beek JG et al. Prognostic value of admission laboratory parameters in traumatic brain injury: results from the IMPACT study. J Neurotrauma. 2007;
Rhoney DH et al. Considerations in fluids and electrolytes after traumatic brain injury. Nutr Clin Pract 2006;21:462–78

6. • Most common electrolyte subject to imbalance –serum sodium
• The most common electrolyte imbalance condition in TBI - hypernatremia
followed by hyponatremia and hypokalemia1
• Calcium disturbance -increased in postoperative period2
• Phosphate and magnesium depletion -severe TBI patients2
1.Suman S, et al. Evaluation of serum electrolytes in traumatic brain injury patients: prospective randomized observational study. J Anesth Crit Care 2016.
2.Lindsey KA,, et al. Influence of traumatic brain injury on potassium and phosphorus homeostasis in critically ill multiple trauma patients. Nutrition 2010

7. Hypernatremia in Traumatic Brain Injury
Patient at risk of developing hypernatremia
• Comorbidities like CHF ,COPD
• Associated alcohol abuse
• More common in males
• Associated coagulopathy
• Asscoiated renal failure
Haydn Hoffman, et al. Effect of Hypernatremia on Outcomes After severe Traumatic Brain Injury: A Nationwide Inpatient Sample
analysis.journal of world neurosurgery. 2018

8. ETIOLOGY
• Iatrogenic
• Insensible water loss
• Hypovolemia
• Diabetes Insipidus (DI)
Haydn Hoffman, Muhammad S. Jalal, Lawrence S. Chin. Effect of Hypernatremia on Outcomes After severe Traumatic Brain Injury: A Nationwide Inpatient
Sample analysis.journal of world neurosurgery. 2018

9. EFFECT
• High rate of renal failure
• Negative effect on cardiac contractility
• Even quick correction- cerebral edema, inc ICP.
Increased the odds of postoperative death in the first 24hours after head injury.
Higher rates of mortality 30.7%vs 26%
Higher LOS
Poor functional outcome in terms of tracheostomy , PEG – those who survive
Haydn Hoffman, et al. Effect of Hypernatremia on Outcomes After severe Traumatic Brain Injury: A Nationwide Inpatient Sample analysis.journal of world
neurosurgery. 2018

10. Diabetes Insipidus
• Most common cause-reported incidence of DI range from 3 to 50%1
• Usually manifest between 4 and 7 days following TBI2
Deficient ADH
 Central DI
 Nephrogenic DI
Usually considered a euvolemic to hypovolemic state
1.Haydn Hoffman, et al.. Effect of Hypernatremia on Outcomes After severe Traumatic Brain Injury: A Nationwide Inpatient Sample analysis.journal of
world neurosurgery. 2018
2.Hannon MJ, et al (2013) Acute glucocorticoid deficiency and diabetes insipidus are common after acute traumatic brain injury and predict mortality. J
Clin Endocrinol Metab .

11. Central Nephrogenic
Hereditary Hereditary
Trauma Electrolyte –hypokalemia, hypercalcemia
Ischemia- sheehan syndrome Drugs- lithium, methoxyflurane
Infection-viral encephalitis, meningitis Amylodosis
Neoplasms- craniopharyngioma, meningioma Postrenal obstruction
Granulomatous diseases- sarcoidosis, histocytosis X

12. DIAGNOSIS
Seckl and Dunger criteria
• Polyuria
• Hypotonic urine
• Increased plasma osmolality
Plasma sodium is more reliable for diagnosis in the acute phase;
plasma sodium concentration > 145 mmol/l
with polyuria
1.Tudor RM, Thompson CJ.Posterior pituitary dysfunction following traumatic brain injury:review. Pituitary;October 2018.
Laboratory Findings
Na >145 mEq/L
Posm > 300 mOsm/kg
Uosm < 300 mOsm/kg
UNa low
Urine Spec. Grav. < 1.005

13. Why diagnosis is important
• DI is so common as a pre-fatal event, that 80% of TBI patients who are brain dead on
ventilators manifest central DI1
• Consistently linked to more severe trauma, cerebral edema, lower GCS scores and a
higher mortality rate2
• The overall mortality -57%–69% and increases to 86%–90% -early-onset of DI3
1.Tudor RM, Thompson CJ.Posterior pituitary dysfunction following traumatic brain injury:review. Pituitary;October 2018.
2.Hadjizacharia, P.; et al, D. Acute diabetes insipidus in severe head injury: A prospective study. J. Am. Coll. Surg. 2008,
3. Karali, V.; et al. Evaluation of development of diabetes insipidus in the early phase following traumatic brain injury in critically ill patients. Crit. Care 2008

14. One Variant
• Triple phasic response
• polyuria 2–4 days ------period of concentration of urine ------hyponatremia, -----------
permanent DI.
Why ? avoid continued Desmopressin therapy in the SIAD phase, which may
worsen hyponatremia.
Hannon MJ et al (2012) Disorders of Water Homeostasis in Neurosurgical Patients. J Clin EndocrinolMetab.1997..

15. Management
• DI is transient
• Goal is to restore plasma volume and serum Na+ levels
• Replace UOP 1:1 with 1/2NS
• Desmopressin Q4-6h, commonly given orally/nasally
• Will be ineffective if nephrogenic (acetazolamide
carbamazepine, clofibrate, chlorpropamide)
1. UPTODATE
2. GREENBERG HANDBOOK OF NEUROSURGERY

16. HYPONATREMIA
• Incidence of hyponatremia following TBI is 33%
ETIOLOGY
• Inadequate sodium intake
• Diuretic use
• SIADH
• Cerebral Salt Wasting Syndrome
Sherlock et al - in 60% of cases . Agha et al -both adults and children
Most cases of SIADH are diagnosed in the first 48 h following TBI, with rare cases
reported up to 18 days following head trauma
Sherlock M, O’Sullivan E, Agha A et al (2009) Incidence and pathophysiology of severe hyponatraemia in neurosurgical patients. Postgrad Med J .
Agha A, Thornton E, O’Kelly P et al (2004) Posterior pituitary dysfunction after traumatic brain injury. J Clin Endocrinol Metab89:5987–5992. https ://doi.org/10.1210/jc.2004-1058

17. Clinical features
• Mild hypo Na+ (120-130)headache,vomiting
• Rapid fall of Na+ (<120mEq/L)coma,seizure, brain
herniation.
• Chronic hypoNa+ (>48hrs)-minimal or nosymptoms
• Rapid fall of Na+ over 12-24hrs(acute hypo Na+ ) may produce neurological symptoms
Meng X, Shi B.Traumatic Brain Injury Patients With a GlasgowComa Scale Score of r8, Cerebral Edema, and/or a Basal Skull Fracture are More Susceptible to Developing
HyponatremiaJournal of Neuroanesthesiology.2015

18. Risk factors
• Traumatic Brain Injury Patients With a GCS Score of 8,
• Cerebral Edema, and/or
• Basal Skull Fracture
Not related to age and sex
Meng X, Shi B.Traumatic Brain Injury Patients With a GlasgowComa Scale Score of r8, Cerebral Edema, and/or a Basal Skull Fracture are More Susceptible to Developing
HyponatremiaJournal of Neuroanesthesiology.2015

19. Mechanisms
• Subarachnoid hemorrhage
• Increased intracranial pressure
• Cerebral edema and local edema
• Basal skull fracture
Meng X, Shi B.Traumatic Brain Injury Patients With a GlasgowComa Scale Score of r8, Cerebral Edema, and/or a Basal Skull Fracture are More Susceptible to
Developing HyponatremiaJournal of Neuroanesthesiology.2015

20. EFFECTS
• Progress to cerebral oedema
• Diminished conscious level, seizures
• poor rehabilitation
• But has not been implicated in excess mortality
Van Beek JG, et al. Prognostic value of admission laboratory parameters in traumatic brain injury: results from the IMPACT study. J
Neurotrauma 2007;
Roxana Maria Tudor· Christopher J. Thompson. Posterior pituitary dysfunction following traumatic brain injury:review. Pituitary.2019 Jun

21. SIADH
• AKA Schwartz-Bartter syndrome,
• release of ADH in the absence of physiologic (osmotic) stimuli
Inappropriate secretion of ADH
 Water excretion is impaired
 Suppression of ADH is impaired

22. DIAGNOSIS
3 criteria- hyponatremia, concentrated urine and no renal/adrenal
dysfunction
Water-load test:Definitive test.
Contraindications: this test is dangerous if the starting serum [Na+] is≤ 124 mEq/L or if
the patient has symptoms of hyponatremia

23. Cerebral Salt Wasting
Renal loss of sodium as a result of intracranial disease, producing hyponatremia
and a decrease in extracellular fluid volume
Two theories:
 Impaired sympathetic neural input
 BNP release
UP TO DATE: Pathophysiology of CSW

24. Diagnosis
Diagnosis:
 Evidence of volume depletion
 Increased urine output
Laboratory Findings
Na < 135 mEq/L
Low Posm
Uosm > 300 mOsm/kg
UNa > 40 mEq/L
High BUN
Increased Cr
Low uric acid
Increased albumin

26. SIADH - treatment
Check serum Na- q 6 hours
Na+ < 125 mEq/L
Severe symptoms No symptoms
3% saline at 1–2 ml/kg body
weight/hr + furosemide 20mg IV
qd/V2 antagonist
NS @ 100 ml/hr + furosemide
20mg IV qd
not exceed 1 mEq/L per hour/ 8 mEq/L in 24 hrs / 18 mEq/L in 48 hrs
UPTO DATE
Fluid restriction is mainstay of therapy
(800ml/day)

27. CSW Treatment
• Treat hypovolemia aggressively.
• Do not give furosemide
• Salt
a) Fludrocortisone acetate Dose: 0.2mg IV or PO q
b) Hydrocortisone
c) Urea: (Ureaphil®) 0.5 grams/kg (dissolve 40 gm in 100–150 ml NS)
IV over 30–60 mins q 8 hrs.

28. Osmotic Demyelination Syndrome
• Cerebral pontine myelinosis + extrapontine myelinosis
• insidious flaccid quadriplegia, mental status changes, and cranial
nerve abnormalities with a pseudobulbar palsy appearance

29. Features common to patients who develop CPM are
• delay in the diagnosis of hyponatremia with resultant respiratory
arrest or seizure with probable hypoxemic event
• rapid correction to normo- or hypernatremia (> 135 mEq/L) within 48
hours of initiating therapy
• increase of serum sodium by > 25 mEq/L within 48 hours of initiation
of therapy
• over-correcting serum sodium
GREENBERG : HANDBOOK OF NEUROSURGERY

30. Management
• Proactive strategy
• Reactive strategy
• Rescue strategy
• Investigational : Minocycline & Dexamethasone
• Experimental : Plasmapharesis
• UP TO DATE :OSMOTIC DEMYLINATION SYNDROME

31. Hyponatremic seizures
• Poorly responsive to anti-convulsants
• » Hypertonic saline(quickly reduce cerebral edema).
• » 1ml/kg of 3% NaCl = 1 mEq/l of Serum Sodium ↑
• » child with active symptoms often improves with 4-6 ml/kg of
3%NaCl
• Need to bring Na to above seizure threshold
• Hypoxia worsens cerebral edema

32. SIADH CSW DI
Serum Na+ < 135 mEq/L < 135 mEq/L > 145 mEq/L
Urine Na+ > 25 mEq/L > 40 mEq/L < 25 mEq/L
Serum Osm < 270 mOsm/kg < 270 mOsm/kg > 285 mOsm/kg
Urine Osm > 300 mOsm/kg > 300 mOsm/kg < 300 mOsm/kg
Urine O/P oliguria polyuria polyuria
CVP normal/high low normal/low
Plasma ADH high normal low
Rx Fluid restrict, give Na+,
vaprisol, demeclocycline
Give volume, give Na+,
fludrocortisone
Drink to thirst, DDAVP
(central), HCTZ
(nephrogenic)

33. Other electrolyte
• Hypokalemia – due to polyuria
• Hypomagnesemia- associated with hypokalemia, TPN, continuous nasogastric
suctioning
• Hypocalcemia-more common in post operative
• Hypophosphetemia
Gupta SK, Ahuja J, Sharma A. Electrolyte imbalanace in traumatic brain injury patients. International Journal of Medical Sciences and Education;2014

34. Take home message
• Neurohypophysial dysfunction is common in the first days following TBI, affecting
approximately 1 in 4 patients.
• Risk of electrolyte abnormalities- Severe head injury
• The most common abnormality following TBI is dysnatremia secondary to SIAD
• 15% of the patients develop DI in the first 48 h following TBI.
• Other electrolyte abnormalities should also be considered.
• Most of these are transient.

35. THANK YOU