Repeat serum sodium levels within a week.
PEARLS AND PITFALLS
- Up to 30% of acute hypernatremia patients will have permanent neurologic sequelae, a complete and well-documented neurologic exam is a must.
- Patients at extreme ages and with chronic conditions are most susceptible to neurologic complications:
- On going fluid losses may require recalculation of fluid needs
- Repeat lab work to confirm controlled correction of sodium
ADDITIONAL READING
- Ellison D. Disorders of sodium and water.
Am J Kidney Dis
. 2005;46(2):356–361.
- Fall P. Hyponatremia and hypernatremia. A systematic approach to causes and their correction.
Postgrad Med
. 2000;107(5):75–82.
- Lin M, Lu S, Lim I. Disorders of water imbalance.
Emerg Med Clin North Am
. 2005;23:749–770, ix.
- Pfennig CL, Slovis CM. Sodium disorders in the emergency department: A review of hyponatremia and hypernatremia.
Emerg Med Pract
. 2012;14(10):1–20.
- Ranadive SA, Rosenthal SM. Pediatric disorders of water balance.
Endocrinol Metabol Clin North Am
. 2009;38(4):663–672.
See Also (Topic, Algorithm, Electronic Media Element)
- Diabetic Ketoacidosis
- Hyperosmolar Coma
- Hyponatremia
CODES
ICD9
- 276.0 Hyperosmolality and/or hypernatremia
- 775.5 Other transitory neonatal electrolyte disturbances
ICD10
- E87.0 Hyperosmolality and hypernatremia
- P74.2 Disturbances of sodium balance of newborn
HYPEROSMOLAR SYNDROME
Matthew T. Robinson
BASICS
DESCRIPTION
- Results from a relative insulin deficiency in the undiagnosed or untreated diabetic
- Sustained hyperglycemia creates an osmotic diuresis and dehydration:
- Extracellular space maintained by the osmotic gradient at the expense of the intracellular space
- Eventually profound intracellular dehydration occurs.
- Total body deficits of H
2
O, Na
+
, Cl
−
, K
−
, PO
4
−
, Ca
2+
, and Mg
2+
- In contrast to diabetic ketoacidosis (DKA), severe ketoacidosis does not occur:
- Circulating insulin levels are higher.
- The elevation of insulin counter-regulatory hormones is less marked.
- The hyperosmolar state itself inhibits lipolysis (the release of free fatty acids) and subsequent generation of keto acids
Geriatric Considerations
- Most commonly seen in elderly type II diabetics who experience a stressful illness that precipitates worsening hyperglycemia and reduced renal function
- In the elderly, 30–40% of cases are associated with the initial presentation of diabetes.
Pediatric Considerations
Hyperosmolar hyperglycemic states (HHS) rare in pediatric patients
ETIOLOGY
- Hyperosmolar state precipitated by factors that:
- Impair peripheral insulin action
- Increase endogenous or exogenous glucose
- Decrease patient’s ability to replace fluid loss
- Infection is the most common precipitating factor in 32–60% of cases.
- Other precipitating causes include:
- Inadequate diabetes therapy
- Medication omission
- Diet indiscretion
- Infections
- Pneumonia
- UTI
- Sepsis
- Medications/drugs
- Diuretics
- β-blockers
- Calcium channel blockers
- Phenytoin
- Cimetidine
- Amphetamines
- Ethanol
- Myocardial infarction
- Stroke
- Renal failure
- Heat stroke
- Pancreatitis
- Intestinal obstruction
- Endocrine disorders
- Burns
- Heat stroke
DIAGNOSIS
SIGNS AND SYMPTOMS
History
- Progression of signs and symptoms typically occur over days to weeks.
- Polyuria/polydipsia/weight loss
- Dizziness/weakness/fatigue
- Blurred vision
- Leg cramps
Physical-Exam
- Dehydration
- Tachycardia
- Sunken eyes
- Hypotension
- Orthostasis
- Dry mucous membranes
- Decreased skin turgor
- Collapsed neck veins
- Coma/lethargy/drowsiness
- Urinary output maintained until late
- Seizures/focal neurologic deficits
- Concurrent precipitating medical illness
ESSENTIAL WORKUP
Diagnostic criteria:
- Serum glucose ≥600 mg/dL (usually >1,000 mg/dL)
- Minimal ketosis
- pH ≥ 7.30, HCO
3
≥15 mEq/L
- Effective serum osmolality >320 mOsm/kg:
- = 2 × Na
+
+ glucose/18
- BUN not included because it is freely permeable between fluid compartments
DIAGNOSIS TESTS & NTERPRETATION
Lab
- Broad testing indicated to evaluate hyperosmolar syndrome and for precipitating causes
- Electrolytes:
- K
+
may be elevated even in the presence of total body deficit owing to shift from intracellular space to extracellular space.
- Mild anion gap metabolic acidosis owing to lactic acid, β-hydroxybutyric acid, or renal insufficiency
- Increased sodium—correct for hyperglycemia: Corrected [Na
+
] = [Na
+
] + 1.6 × [(glucose in mg/dL) – 100]/100
- BUN, creatinine:
- Azotemia with elevated BUN/creatinine ratio owing to prerenal and intrarenal causes
- Venous blood gas (VBG) or arterial blood gas (ABG) to rapidly determine pH:
- ABG necessary to evaluate mixed acid–base disorders
- Serum ketones, β-hydroxybutyrate, and lactate level if pH < 7.3 or significantly elevated anion gap to evaluate mixed acid–base disorder
- Serum osmolarity
- CBC:
- Leukocytosis due to infection, stress, or hemoconcentration
- Increased hemoglobin and hematocrit due to hemoconcentration
- Lipase and amylase:
- Pancreatitis common
- Elevated amylase and lipase with no evidence of pancreatitis common
- May be due to increased salivary secretion, hemoconcentration, or decreased renal clearance
- Urinalysis:
- Check for ketones/glucose.
- Assess for UTI.
- Magnesium, calcium, phosphate
- Blood cultures in sepsis
- Creatine kinase for rhabdomyolysis:
- Urine pregnancy test in females of childbearing years
- Cardiac enzymes and troponin for myocardial infarction
Imaging
- CXR to evaluate for possible underlying pneumonia
- Head CT: When indicated for AMS or with focal neurologic deficit
Diagnostic Procedures/Surgery
ECG:
- Evaluate for electrolyte abnormalities causing conduction impairment
- Evaluate for signs of ischemia as triggering event
DIFFERENTIAL DIAGNOSIS
Differentiate from DKA:
- If acidosis or significant anion gap present, must determine cause (i.e., ketosis, DKA, lactic acidosis, [hypoperfusion, sepsis, or postictal], or other causes of metabolic acidosis)
- Mixed disorder of HHS and DKA present in up to 33% of patients
TREATMENT
PRE HOSPITAL
IV fluid resuscitation and initial stabilization
INITIAL STABILIZATION/THERAPY