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432 Laboratory Medicine in Psychiatry and Behavioral Science
Hyperglycemia
Clinical findings Hyperglycemia is defined by the following blood glucose levels:
• >125 mg/dL in the fasting state
• >180 mg/dL 2 hours after eating
Diabetes—the most common cause of persistent hyperglycemia—is
discussed separately in the Diabetes Mellitus entry.
Other causes of hyperglycemia include the following:
• Acute stress response (e.g., in critical illness or postoperative state)
•Pregnancy
• Pancreatic tissue destruction from chronic pancreatitis, cystic fi-
brosis, cancer, or hemochromatosis
• Endocrine disorders causing insulin resistance, such as Cushing’s
syndrome, acromegaly, and pheochromocytoma
• Use of drugs such as diuretics, corticosteroids, phenytoin, TCAs,
β-blockers, dextrothyroxine, epinephrine, estrogens, glucagon, iso-
niazid, lithium, or phenothiazines
• Chronic renal failure
•Glucagonoma
• Total parenteral nutrition with dextrose infusion
Signs and symptoms of hyperglycemia include polydipsia, polyuria,
hypotension, tachycardia, headache, and blurred vision. With per
-
sistence and further elevation, altered mental status, lethargy, and fo-
cal neurological signs may be observed.
Laboratory testing The panic value for glucose in both males and females is >400 mg/dL.
Dipstick urinalysis can return quick results for glucose and ketones in
urine.
Other laboratory tests include serum electrolytes, BUN, creatinine, and
CBC. Blood gases may be required if serum bicarbonate is significantly
reduced. Serum and urine osmolality help diagnose diabetic ketoaci
-
dosis and hyperglycemic hyperosmolar nonketotic state.
Marik PE, Bellomo R: Stress hyperglycemia: an essential survival response!Crit Care 17(2):305, 2013
Mouri M, Badireddy M: Hyperglycemia, in StatPearls. Treasure Island, FL, StatPearls Publishing, 2022.
Available at: https://www.ncbi.nlm.nih.gov/books/NBK430900
. Accessed April 2022.
Perez A, Jansen-Chaparro S, Saigi I, et al: Glucocorticoid-induced hyperglycemia.J Diabetes 6(1):9–20,
2014
Pratiwi C, Zulkifly S, Dahlan TF, et al: Hospital related hyperglycemia as a predictor of mortality in non-
diabetes patients: a systematic review.Diabetes Metab Syndr 15(6):102309, 2021
Roszali MA, Zakaria AN, Mohd Tahir NA: Parenteral nutrition-associated hyperglycemia: prevalence,
predictors and management. Clin Nutr ESPEN 41:275–280, 2021
Scheen M, Giraud R, Bendjelid K: Stress hyperglycemia, cardiac glucotoxicity, and critically ill patient
outcomes current clinical and pathophysiological evidence.Physiol Rep 9(2):e14713, 2021
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433 Diseases and Conditions
Hyperkalemia
Clinical findings Hyperkalemia is defined by a serum potassium level >5 mEq/L. Cal-
cium elevation occurs because of reduced renal excretion (persistent
elevation) and/or a shift of intracellular potassium to the extracellular
space (transient elevation).
Causes of hyperkalemia include the following:
• Chronic renal failure/insufficiency
• Systemic illness, dehydration, or the introduction of potassium-
elevating drugs
• Increased potassium intake in patients with renal insufficiency
• Tissue injury: trauma, burns, tumor lysis, massive hemolysis, or
rhabdomyolysis
• Insulin deficiency
• Exercise in the presence of β-blockers
• Hyperchloremic metabolic acidosis with a normal anion gap
• Hypertonic states such as hyperglycemia
• Endocrine disease such as Addison’s disease or primary hypoaldo-
steronism
•SLE
• Drugs:
ACE inhibitors, angiotensin receptor blockers, potassium-
sparing diuretics, potassium salts, succinylcholine, NSAIDs, and
certain laxatives
Signs and symptoms of hyperkalemia include bradycardia, weakness,
ileus or diarrhea, low urine output, muscular irritability, tremors, fas
-
ciculations, paresthesias, and flaccid paralysis. The latter is an ascend-
ing paralysis leading to flaccid quadriplegia with sparing of the trunk,
head, and respiratory muscles. Characteristic ECG changes are listed
in the Laboratory Testing section below.
Hyperkalemia can represent a medical emergency. Factors determin-
ing severity include not only the level of elevation but also the rapidity
with which it develops and the duration of elevation. Patients with a
rapid rise in serum potassium, ECG changes, reduced renal function,
or significant acidosis must be treated urgently.
Laboratory testing Spurious elevation of potassium can occur, mostly related to specimen
handling and transport problems, as noted in the Potassium entry in
the Laboratory Tests chapter. Spurious elevation can be suspected
when a patient has normal renal function, normal serum bicarbonate,
and/or a normal ECG. Spurious elevation can be confirmed by repeat-
ing potassium measurements in both serum and plasma; in this case,
the serum potassium will be elevated but the plasma potassium will
be normal.
In addition to close monitoring of the potassium level, laboratory tests
include the following:
•ECG
•BUN and creatinine
• Electrolytes
• Spot urine testing for potassium, creatinine, and osmoles
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434 Laboratory Medicine in Psychiatry and Behavioral Science
Hyperkalemia (continued)
Laboratory testing
(continued)
ECG changes emerge when the potassium level is ≥6.0 mEq/L, al-
though threshold depends in part on the rate of rise. Progression of
ECG changes is as follows:
• Tall, peaked T waves (higher than R waves)
• ST segment depression
• Prolonged PR interval
• QRS widening
• Reduced or absent P waves
• Sine wave pattern: impending ventricular fibrillation and asystole
Ben Salem C, Badreddine A, Fathallah N, et al: Drug-induced hyperkalemia.Drug Saf 37(9):677–692, 2014
Hollander-Rodriguez JC, Calvert JF Jr: Hyperkalemia.Am Fam Physician 73(2):283–290, 2006
Littmann L, Gibbs MA: Electrocardiographic manifestations of severe hyperkalemia.J Electrocardiol
51(5):814–817, 2018
Montford JR, Linas S: How dangerous
is hyperkalemia?J Am Soc Nephrol 28(11):3155–3165, 2017
Palmer BF, Clegg DJ: Diagnosis and treatment of hyperkalemia.Cleve Clin J Med 84(12):934–942, 2017
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435 Diseases and Conditions
Hypermagnesemia
Clinical findings Hypermagnesemia is defined by a serum magnesium level > 2.6 mg/dL.
It usually occurs in the presence of renal insufficiency or failure, often
in an elderly patient with recent ingestion of magnesium-containing
laxatives or antacids. Although it is not a common derangement, it can
be fatal if it remains untreated.
Causes of hypermagnesemia include the following:
•
Decreased renal excretion (acute or chronic renal insufficiency or
failure)
•
Hyperparathyroidism
• Drugs: lithium, certain antacids, certain laxatives
• Increased intake of laxatives, antacids, bowel preps
• Milk-alkali syndrome
• Treatment of eclampsia with IV magnesium sulfate
•
Compartment shift: hemolysis, tumor lysis, rhabdomyolysis, aci-
dosis
The risk of developing hypermagnesemia is heightened in the pres-
ence of alcohol use disorder, malnutrition, hypothyroidism, and adre-
nal insufficiency.
Signs and symptoms of hypermagnesemia include the following:
• Mild elevation (<7 mg/dL): asymptomatic or nonspecific symp-
toms of nausea, dizziness, weakness, and confusion
• Moderate elevation (7–12 mg/dL): hypotension, bradycardia,
blurred vision, psychomotor retardation, hyporeflexia, sleepiness,
worsening confusion, headache, flushing, constipation, and blad
-
der dysfunction
• Severe elevation (>12 mg/dL): worsening hypotension and brady-
cardia, arrhythmias, ECG changes, flaccid paralysis, respiratory
depression, and lethargy
• Very severe elevation (>15 mg/dL): cardiorespiratory arrest and
coma
Laboratory testing Normal serum magnesium levels:
• <60 years: 1.6–2.6 mg/dL
• 60–90 years: 1.6–2.4 mg/dL
• >90 years: 1.7–2.3 mg/dL
Laboratory evaluation for suspected hypermagnesemia includes the
following:
•
Serum magnesium level
• ECG
• Renal evaluation: BUN, creatinine, eGFR, urine specific gravity
• Arterial blood gases
• Urine output quantification
• Potassium, phosphate, and calcium levels (serum and urine)
Barra A, Camardese G, Tonioni F, et al: Plasma magnesium level and psychomotor retardation in major
depressed patients. Magnes Res 20(4):245–249, 2007
Bokhari SR, Siriki R, Teran FJ, Batuman V: Fatal hypermagnesemia due to laxative use.Am J Med Sci
355(4):390–395, 2018
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436 Laboratory Medicine in Psychiatry and Behavioral Science
Hypermagnesemia (continued)
Brackenridge CJ, Jones IH: Relation of hypermagnesaemia to activity and neuroleptic drug therapy in
schizophrenic states.J Neurol Neurosurg Psychiatry 34(2):195–199, 1971
Felsenfeld AJ, Levine BS, Rodriguez M: Pathophysiology of calcium, phosphorus, and magnesium dys-
regulation in chronic kidney disease. Semin Dial 28(6):564–577, 2015
Sawalha K, Kakkera K: Acute respiratory failure from hypermagnesemia requiring prolonged mechani-
cal ventilation. J Investig Med High Impact Case Rep 8:2324709620984898, 2020
Stevens JS, Moses AA, Nickolas TL, et al: Increased mortality associated with hypermagnesemia in severe
COVID-19 illness.Kidney360 2(7):1087–1094, 2021
Takahashi M, Uchino N: Risk factors of hypermagnesemia in end-stage cancer patients hospitalized in a
palliative care unit.Ann Palliat Med 9(6):4308–4314, 2020
Van Laecke S: Hypomagnesemia and hypermagnesemia.Acta Clin Belg 74(1):41–47, 2019
Walker P, Parnell S, Dillon RC: Epsom salt ingestion leading to severe hypermagnesemia necessitating
dialysis.J Emerg Med 58(5):767–770, 2020
Yamaguchi H, Shimada H, Yoshita K, et al: Severe hypermagnesemia induced by magnesium oxide in-
gestion: a case series.CEN Case Rep 8(1):31–37, 2019
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437 Diseases and Conditions
Hypernatremia
Clinical findings Hypernatremia is defined by a serum sodium concentration >145 mEq/
L. It represents a state of total body water deficiency, either absolute or
relative to total body sodium (and potassium). It is a consequence of
water loss, hypotonic fluid loss, or hypertonic fluid gain. It is more com-
mon in elderly patients, those lacking the ability to monitor their thirst
and drinking behavior, and in those who are critically ill. This is a po
-
tentially serious condition, particularly
large or occurs rapidly. The short-term mortality rate is as high as 60%.
Usually, the cause of hypernatremia becomes apparent with the history
and physical exam. Most cases result from water loss, either through the
kidneys (diabetes insipidus), GI tract (vomiting or osmotic diarrhea),
lungs (hyperventilation), or skin (diaphoresis). Cases resulting from hy
-
pertonic fluid gain are usually iatrogenic. On psychiatry services, hyper-
natremia occurs with lithium use (nephrogenic diabetes
excessive fluid loss (significant vomiting or diarrhea), and the use of
restraints or seclusion rooms where access to water is
Adult patients may be asymptomatic or may exhibit signs of CNS dys-
function such as irritability, somnolence, restlessness, weakness, nausea,
chorea, myoclonus, myalgia, muscle cramps, altered mental status, de-
lirium, or coma. The level of consciousness is correlated with the degree
of hypernatremia. Hypovolemia is associated with orthostatic hypoten
-
sion and tachycardia. Cellular dehydration causes brain shrinkage, with
complications such as subdural hematoma and intracerebral hemor
-
rhage that may cause permanent brain injury or death. Further compli-
cations include seizures and rhabdomyolysis.
Laboratory testing In the evaluation of the patient who presents with hypernatremia
(sodium>145 mEq/L), the first question to ask is why the patient is not
drinking water. Nursing home patients with cognitive impairment, for
example, might be relying on others to provide fluids.
An algorithm for the workup of hypernatremia is as follows:
•
If the physical exam demonstrates hypovolemia or euvolemia, as-
sess urine flow rate.
•
A urine flow rate ≥ 30 mL/hour indicates renal loss of hypotonic
fluid.
•
A urine flow rate <30 mL/hour indicates hypotonic fluid loss from
outside the kidney.
• With renal loss, check urine osmolality.
• Urine osmolality >300 mOsm/kg H
2
0 indicates osmotic diuresis.
• Urine osmolality <300 mOsm/kg H
2
0 indicates water diuresis.
• In the case of water diuresis, check either the copeptin level or
plasma osmolality to compare with urine osmolality in order to
distinguish central from nephrogenic diabetes insipidus.
Adrogué HJ, Madias NE: Hypernatremia.N Engl J Med 342(20):1493–1499, 2000
Braun MM, Barstow CH, Pyzocha NJ: Diagnosis and management of sodium disorders: hyponatremia
and hypernatremia. Am Fam Physician 91(5):299–307, 2015
Kamel KS, Schreiber M, Harel Z: Hypernatremia. JAMA 327(8):774–775, 2022
Liamis G, Filippatos TD, Elisaf MS: Evaluation and treatment of hypernatremia: a practical guide for phy-
sicians. Postgrad Med 128(3):299–306, 2016
Muhsin SA, Mount DB: Diagnosis and treatment of hypernatremia. Best Pract Res Clin Endocrinol Metab
30(2):189–203, 2016
Qian Q: Hypernatremia. Clin J Am Soc Nephrol 14(3):432–434, 2019
Reynolds RM, Padfield PL, Seckl JR: Disorders of sodium balance. BMJ 332:702–705, 2006
https://t.me/med1917
438 Laboratory Medicine in Psychiatry and Behavioral Science
Hyperparathyroidism
Clinical findings Primary hyperparathyroidism (PHPT), characterized by mild to mod-
erate elevation of serum calcium levels with non-suppressed or high
levels of PTH, is most often caused by a single parathyroid adenoma.
The disease primarily targets the kidneys and the skeleton, causing
kidney stones and cortical bone loss with increased risk of fracture. It
is also associated with an increased risk of hypertension and cardiac
changes that may have a fatal outcome. Neuropsychiatric symptoms
including anxiety, depression, poor concentration, and memory im
-
pairment are often reported. PHPT is relatively common, particularly
in females older than 50 years. It is usually discovered when slightly
elevated calcium is found on routine chemistry testing. At this stage,
the patient is usually asymptomatic but may present with kidney
stones, bone pain, or fracture. Long-term treatment with lithium can
mimic PHPT laboratory values.
Laboratory testing Laboratory evaluation for PHPT includes the following:
• Ionized or corrected serum calcium (elevated)
• Intact PTH level (normal or elevated)
• 25-hydroxyvitamin D level (normal or low-normal)
• GFR (normal)
• 24-hour urine calcium excretion (elevated)
• Bone density evaluation including the distal third of the radius
• Renal ultrasound to detect stones
Bilezikian JP, Bandeira L, Khan A, Cusano NE: Hyperparathyroidism.Lancet 391(10116):168–178, 2018
Clarke BL: Asymptomatic primary hyperparathyroidism. Front Horm Res 51:13–22, 2019
Insogna KL: Primary hyperparathyroidism.
Khan AA, Hanley DA, Rizzoli R, et al: Primary hyperparathyroidism: review and recommendations on
evaluation, diagnosis, and management: a Canadian and international consensus.Osteoporos Int
28(1):1–19, 2017
Masi L: Primary hyperparathyroidism.Front Horm Res 51:1–12,
Walker MD, Bilezikian JP: Primary hyperparathyroidism: recent advances.Curr Opin Rheumatol
30(4):427–439, 2018
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439 Diseases and Conditions
Hypertensive encephalopathy
Clinical findings
Laboratory testing
Hypertensive encephalopathy is a clinical syndrome associated with
the subacute onset of extreme hypertension, with a systolic blood
pressure often >220 mmHg or a diastolic blood pressure >130 mmHg.
The degree of hypertension required to develop the syndrome in a
given patient depends on their premorbid blood pressure; for example,
a previously normotensive person could develop encephalopathy at
blood pressures of 160/100 mmHg. Hypertensive encephalopathy is a
medical emergency requiring immediate treatment to lower blood
pressure in all patients.
The mechanism by which hypertension causes encephalopathy is
thought to be a failure of autoregulation in the cerebral vasculature
when the upper limit of autoregulation is exceeded, usually when the
diastolic blood pressure exceeds 120 mmHg. At that point, massive
constriction and reflex vasodilation of cerebral arterioles occur, giving
rise to vasogenic edema that can be seen on neuroimaging.
This syndrome overlaps with posterior reversible encephalopathy syn-
drome (PRES), which has more region-specific pathology either in the
posterior supratentorial structures or the brainstem. PRES can also be
identified in normotensive individuals in whom autoimmune disease,
sepsis, renal disease, preeclampsia, or the use of cytotoxic drugs has
caused vascular injury.
Clinical presentation often involves a patient with chronically uncon-
trolled hypertension who recently stopped antihypertensive therapy.
Underlying causes include acute or chronic kidney disease, autoim
-
mune disorders, endocrine disorders, porphyria, thermal injury, TBI,
autonomic hyperactivity, scorpion envenomation, cocaine or amphet-
amine abuse, tyramine reactions with MAOI treatment, and use of
stimulants such as ephedrine, pseudoephedrine, or caffeine.
Signs and symptoms of hypertensive encephalopathy typically in-
clude gradual onset of headache, nausea, and vomiting followed by
neuropsychiatric symptoms of restlessness, confusion, delirium,
stupor, seizures, and, in some cases, coma. Papilledema and visual
changes may be noted. When neurological deficits are seen, they are
not localized in the same manner as with PRES or a space-occupying
lesion but instead indicate global cerebral dysfunction. End-organ
injury from hypertension may also be seen in the kidneys, heart, and
retinas, the latter showing retinal hemorrhages and exudates.
The diagnosis of hypertensive encephalopathy is based on clinical
findings, but neuroimaging can be helpful by demonstrating the pres-
ence of vasogenic cerebral edema. MRI with T2-weighted and FLAIR
sequences is preferred to CT for this purpose.
Lumbar puncture may be performed to assist in the differential diag-
nosis of encephalopathy. Mild to modestly elevated protein levels
without pleocytosis can be seen. Elevated intracranial pressure may be
noted.
Other diagnostic procedures may be needed to evaluate end-organ in-
jury and identify potential causes of secondary hypertension, includ-
ing ECG, chest X-ray or CT, urinalysis, cardiac enzymes, and BMP or
CMP. Serum or urine pregnancy testing should be performed for pa-
tients of childbearing age. Urine drug screening should be considered
if there is concern about stimulant use, but this will not detect over-the-
counter drugs.
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440 Laboratory Medicine in Psychiatry and Behavioral Science
Hypertensive encephalopathy (continued)
Christopoulou F, Rizos EC, Kosta P, et al: Does this patient have hypertensive encephalopathy?J Am Soc
Hypertens 10(5):399–403, 2016
Dunphy L, Kothari T, Ford J: Posterior reversible encephalopathy syndrome in the puerperium: a case
report. BMJ Case Rep 15(1):e246570, 2022
Fischer M, Schmutzhard E: Posterior reversible encephalopathy syndrome. J Neurol 264(8):1608–1616,
2017
Gewirtz AN, Gao V, Parauda SC, Robbins MS: Posterior reversible encephalopathy syndrome.Curr Pain
Headache Rep 25(3):19, 2021
Gifford RW Jr, Westbrook E: Hypertensive encephalopathy: mechanisms, clinical features, and treatment.
Prog Cardiovasc Dis 17:115–124, 1974
Miller JB, Suchdev K, Jayaprakash N, et al: New developments in hypertensive encephalopathy.Curr
Hypertens Rep 20(2):13, 2018
Tan YY, Tan K: Hypertensive brainstem encephalopathy: a diagnosis often overlooked.Clin Med (Lond)
19(6):511–513, 2019
Thambisetty M, Biousse V, Newman NJ: Hypertensive brainstem encephalopathy: clinical and radio-
graphic features. J Neurol Sci 208:93–99, 2003
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441 Diseases and Conditions
Hypocalcemia
Clinical findings
Laboratory testing
Calcium is an essential micronutrient with important roles in neuro-
transmission, cardiac function, muscle contraction, blood clotting, and
bone formation. The calcium level is maintained within a physiological
range through the actions of PTH and vitamin D. Only ~1% of the
body’s calcium is in circulation, half bound to albumin and half in the
free or ionized form. When the albumin level drops, the total calcium
level drops as well, but the concentration of free calcium is unaffected.
For this reason, the total calcium value is corrected when the albumin
level is low, using the formula corrected calcium=[4 g/dL−plasma
albumin]×0.8+total serum calcium. Alternatively, free calcium can be
measured directly, but in this case, the specimen requires special han
-
dling and expedited processing.
Hypocalcemia is defined by a corrected total calcium level≤ 8 mg/dL
and/or the presence of symptoms. The primary causes of hypocalce
-
mia can be divided into PTH-mediated and non-PTH-mediated, the
former represented by parathyroid deficiency after thyroid or parathy
-
roid surgery and the latter by vitamin D deficiency. Risk factors for
deficiency of vitamin D include limited sun exposure, skin pigmenta-
tion, and age-related thinning of the skin.
Other causes of hypocalcemia include acute pancreatitis, renal failure,
malnutrition, malabsorption due to GI disease, elevated phosphate
levels (e.g., from laxative abuse), severe osteomalacia, and the use of
drugs such as bisphosphonates, cisplatin, antiepileptics, diuretics,
aminoglycosides, or proton pump inhibitors.
The signs and symptoms of hypocalcemia depend on the rapidity of
its development and the severity of the calcium reduction. Acutely de-
veloping hypocalcemia can be a medical emergency, with delirium,
seizures, cardiac arrhythmias, QT prolongation, heart failure, laryngo
-
spasm, and bronchospasm. Almost any organ system can be affected,
and the condition can be life-threatening.
In contrast, gradually developing hypocalcemia can be asymptomatic,
discovered only on routine health screening, or can be characterized
by signs of neuromuscular irritability such as paresthesias, muscle
twitching and spasm, and tetany. Carpopedal spasm is a classic sign.
When neuromuscular signs are not apparent, they can sometimes be
elicited by provocations such as tapping on the facial nerve just in front
of the tragus to induce twitching of the mouth (Chvostek’s sign) or
inflating a blood pressure cuff above the systolic pressure for ≤3 min-
utes to induce carpal spasm (Trousseau’s sign). Other signs and symp-
toms include anxiety, depression, irritability, fatigue, apathy, lethargy,
weakness, anorexia, nausea, vomiting, constipation, polyuria, poly
-
dipsia, bone pain, and seizures. Chronic hypocalcemia can be associ-
ated with calcification in the lens of the eye, basal ganglia, cerebellum,
and cerebral cortex.
An acute drop in total serum calcium to 8 mg/dL may cause symp-
toms, whereas gradual decline to 7 mg/dL may be asymptomatic.
Most patients show symptoms when total calcium is at or around
6 mg/dL (ionized calcium <2 mg/dL). At this level and below, tetany
and seizures are seen.
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