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442 Laboratory Medicine in Psychiatry and Behavioral Science
Hypocalcemia (continued)
Laboratory testing
(continued)
To diagnose the cause of hypocalcemia, initial laboratory testing
includes the following:
•
Serum calcium (corrected)
• Electrolyte panel
• Phosphate
• Magnesium
• Creatinine
• ALP
• PTH
• 25-hydroxy vitamin D
• Serum pH
• CBC
Cooper and Gittoes (2008; see below) offered a useful chart to help
identify the cause of hypocalcemia with the results of these initial tests.
Further investigations may include ionized calcium, renal ultrasound,
1,25-dihydroxy vitamin D, and 24-hour urinary measures of phos
-
phate, calcium, magnesium, and creatinine. Testing for genetic muta-
tions and evaluation of first-degree relatives may be indicated.
Calpena Martínez S, Arapiles Muñoz A: The value of the classic signs: hypocalcemia.Med Clin (Barc)
157(11):554, 2021
Cooper MS, Gittoes NJ: Diagnosis and management of hypocalcaemia. BMJ 336(7656):1298–1302, 2008
[published correction appears in BMJ 336(7659), 2008]
Fong J, Khan A: Hypocalcemia: updates in diagnosis and management for primary care.Can Fam Phy-
sician 58(2):158–162, 2012
Giusti F, Brandi ML: Clinical presentation of hypoparathyroidism. Front Horm Res 51:139–146, 2019
Hakami Y, Khan A: Hypoparathyroidism.Front Horm Res 51:109–126, 2019
Lawlor BA: Hypocalcemia, hypoparathyroidism, and organic anxiety syndrome. J Clin Psychiatry 49(8):317–
318, 1988
Pepe J, Colangelo L, Biamonte F, et al: Diagnosis and management of hypocalcemia. Endocrine 69(3):485–
495, 2020
Sapountzi P, Emanuele NV, Loutrianakis E, et al: Vi sual vignette. Diagnosis: hypocalcemia due to pri-
mary hypoparathyroidism. Endocr Pract 12:233, 2006
Teisseyre M, Moranne O, Renaud S: Late diagnosis of chronic hypocalcemia due to autoimmune hypo-
parathyroidism. BMJ Case Rep 14(6):e243299, 2021
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443 Diseases and Conditions
Hypoglycemia
Clinical findings Hypoglycemia is most often seen in patients treated for diabetes. Initial
autonomic symptoms include hunger, sweating, palpitations, tremor,
anxiety, and paresthesias. Without intervention, a further decline in glu
-
cose may result in brain glucose deprivation, with symptoms such as the
following:
• Behavioral changes, including agitation and aggression
• Irritability
• Depersonalization
• Panic attacks
• Confusion
• Blurred vision
• Slurred speech
• Dizziness
• Fatigue, lethargy
• Headache
• Transient focal neurological deficits
• Seizures
• Loss of consciousness, coma
Because these symptoms are not specific to hypoglycemia, it is import-
ant to establish and document a link between the two before initiating
a workup to determine the underlying cause. Not only should charac
-
teristic symptoms and low blood glucose values be present, but symp-
toms should resolve with correction of glucose. It may be necessary to
simulate the conditions under which hypoglycemia is said to have oc
-
curred. For example, if the problem is postprandial, a meal should be
provided, followed by glucose testing. The general rule of thumb,
however, is that any person with diabetes who is taking antidiabetic
medication and whose behavior is in any way odd is considered hypo
-
glycemic until proven otherwise.
Among insulin-treated diabetics, the annual incidence of hypoglyce-
mia is up to 40% of those with type 1 diabetes and up to 30% of those
with type 2 diabetes. Oral drugs for diabetes can also cause hypogly-
cemia, as can anabolic steroids, propranolol, and MAOIs. Non-drug
causes include the following:
• Insulinoma
• Hypothyroidism
• Hypopituitarism
• Addison’s disease
• Autoimmune disease
• Alcohol use disorder
• Severe liver disease
• End-stage renal disease
• Post–bariatric surgery state
• Starvation, fasting, anorexia nervosa
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444 Laboratory Medicine in Psychiatry and Behavioral Science
Hypoglycemia (continued)
Clinical findings The risk of developing hypoglycemia is highest in elderly patients and
(continued) in those with multiple comorbidities, a long duration of diabetes, or a
prior history of hypoglycemia, even if mild. Dietary factors such as
delaying or skipping meals or inadequate consumption of carbohy
-
drates
The sequelae of hypoglycemia depend on the severity and duration
of the deficiency. Severe hypoglycemia can cause brain injury, coma,
and death if not treated emergently. Mild hypoglycemia, when pro
-
longed, can cause peripheral nerve injury. Recurrent hypoglycemia is
associated with cognitive deficits, particularly in executive function,
and current hypoglycemia with attentional and memory impairment.
Nocturnal hypoglycemia may increase the risk of cardiac events be
-
cause blood sugar values at night can be very low and of long dura-
tion and may not easily be detected.
Laboratory testing Glucose values requiring urgent intervention:
• Males: <50 mg/dL
• Females: <40 mg/dL
The lower limit of normal for fasting glucose is ~ 70 mg/dL, but lower
levels can occur normally after meals. Various definitions of hypo-
glycemia set the glucose threshold at slightly different levels. One
reasonable definition is as follows: glucose level <55 mg/dL (by a
reliable method) with characteristic symptoms that are relieved when
glucose level is raised. Glucose monitors are not considered reliable
gauges at low glucose levels.
While the patient is symptomatic, check
• Blood glucose (<55 mg/dL)
• Insulin level (considered increased if >6 μL/mL)
If factitious disorder is suspected, C peptide level can be checked. Both
insulin level and C peptide level ar
oral hypoglycemic drugs (as well as with insulinomas). Cpeptide level
is decreased with exogenous insulin use.
Endocrinology consultation is recommended to determine what other
tests are needed to investigate the underlying cause of hypoglycemia.
Benton D: Hypoglycemia and aggression: a review. Int J Neurosci 41:163–168, 1988
Galati SJ, Rayfield EJ: Approach to the patient with postprandial hypoglycemia. Endocr Pract 20(4):331–
340, 2014
Grunberger G, Weiner JL, Silverman R, et al: Factitious hypoglycemia due to surreptitious administration
of insulin: diagnosis, treatment, and long-term follow-up. Ann Intern Med 108:252–257, 1988
Languren G, Montiel T, Julio-Amilpas A, Massieu L: Neuronal damage and cognitive impairment asso-
ciated with hypoglycemia: an integrated view. Neurochem Int 63(4):331–343, 2013
McNay EC, Cotero VE: Mini-review: impact of recurrent hypoglycemia on cognitive and brain function.
Physiol Behav 100:234–238, 2010
Mohseni S: Neurologic damage in hypoglycemia.Handb Clin Neurol 126:513–532, 2014
Muneer M: Hypoglycaemia. Adv Exp Med Biol 1307:43–69, 2021
Murad MH, Coto-Yglesias F, Wang AT, et al: Clinical review: drug-induced hypoglycemia: a systematic
review. J Clin Endocrinol Metab 94:741–745, 2009
Scarlett JA, Mako ME, Rubenstein AH, et al: Factitious hypoglycemia: diagnosis by measurement of se-
rum C-peptide immunoreactivity and insulin-binding antibodies. N Engl J Med 297:1029–1032, 1977
Umpierrez G, Korytkowski M: Diabetic emergencies: ketoacidosis, hyperglycaemic hyperosmolar state
and hypoglycaemia.Nat Rev Endocrinol 12(4):222–232, 2016
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445 Diseases and Conditions
Hypogonadism
Clinical findings Hypogonadism is a syndrome of sex hormone deficiency affecting
both males and females. Menopause (and its counterpart in males) is
the most common cause of this condition.
Pathological causes are classified as primary or secondary. In primary
hypogonadism, the problem resides with the testes or ovaries. In sec
-
ondary (central) hypogonadism, the problem resides with the hypo-
thalamus or pituitary gland. Primary hypogonadism can be genetic or
can be the consequence of autoimmune disease, infection, liver dis
-
ease, kidney disease, radiation to the gonads, surgery, or trauma. The
most common genetic causes are Turner’s syndrome in females and
Klinefelter syndrome in males. Secondary hypogonadism causes in
-
clude anorexia nervosa, pituitary hemorrhage, infection, malnutrition,
hemochromatosis, radiation to the pituitary or hypothalamus, rapid
significant weight loss, surgery adjacent to the pituitary gland, tumors,
trauma, and drugs such as cortisol and opioids. Stopping high doses
of anabolic steroids can result in very low testosterone levels. Kall-
mann syndrome is a genetic cause of secondary hypogonadism.
Children with hypogonadism do not develop normally in terms of pri-
mary and secondary sexual characteristics. When hypogonadism de-
velops after puberty, symptoms include the following:
• In females: hot flashes, energy and mood changes, insomnia, irreg-
ular or absent menstruation, infertility
• In males: hot flashes, lethargy, depression, low libido, erectile dys-
function, gynecomastia, loss of muscle mass, loss of body hair, tes-
ticular atrophy, oligospermia, and reduced bone density
Other signs and symptoms may be seen with secondary hypogonad-
ism, including visual loss, headaches, breast discharge (from prolacti-
noma), and symptoms of other hormonal deficiencies such as
hypothyroidism.
Laboratory testing In females age 45 years and older, symptoms typical of menopause are
not an indication for laboratory testing. Estradiol levels are checked for
symptoms occurring in females younger than 45 years, in undernour
-
ished patients with unexplained amenorrhea, and in the workup for
infertility. In these cases, FSH and LH are checked along with estradiol.
Primary hypogonadism is diagnosed when estradiol (and progester-
one) levels are low but FSH and LH levels are normal or high. Second-
ary hypogonadism is diagnosed when
estradiol (and progesterone)
levels as well as FSH and LH levels are low.
In males with symptoms of testosterone deficiency, testosterone level
is checked (between 8:00
A.M. and 11:00 A.M.) along with LH and FSH.
If the testosterone level is <200 ng/dL, the level is rechecked. If the
level is 200–400 ng/dL, free testosterone level is checked. If the level is
≥ 400 ng/dL, the result is normal. Primary hypogonadism is diagnosed
by low testosterone, elevated LH, and elevated FSH. Secondary hypo-
gonadism is diagnosed by low testosterone, normal or low LH, and
normal or low FSH.
Additional tests may be indicated depending on results, including
CBC and iron studies, prolactin level, thyroid function tests, ACTH,
sperm count, sex hormone binding globulin, ultrasound of the ovaries,
and brain MRI or head CT.
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446 Laboratory Medicine in Psychiatry and Behavioral Science
Hypogonadism (continued)
Alwani M, Yassin A, Talib R, et al: Cardiovascular disease, hypogonadism and erectile dysfunction: early
detection, prevention and the positive effects of long-term testosterone treatment: prospective obser
-
vational, real-life data.Vasc Health Risk Manag 17:497–508, 2021
Dobs AS: The role of accurate testosterone testing in the treatment and management of male hypogonad-
ism. Steroids 73:1305–1310, 2008
Hall SA, Esche GR, Araujo AB, et al: Correlates of low testosterone and symptomatic androgen deficiency
in a population-based sample. J Clin Endocrinol Metab 93:3870–3877, 2008
Khera M, Broderick GA, Carson CC III, et al: Adult-onset hypogonadism.Mayo Clin Proc 91(7):908–926,
2016
Livingston M, Kalansooriya A, Hartland AJ, et al: Serum testosterone levels in male hypogonadism: why
and when to check—a review.Int J Clin Pract 71(11):e12995, 2017
Richard-Eaglin A: Male and female hypogonadism. Nurs Clin North Am 53(3):395–405, 2018
Salonia A, Rastrelli G, Hackett G, et al: Paediatric and adult-onset male hypogonadism.Nat Rev Dis
Primers 5(1):38, 2019
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447 Diseases and Conditions
Hypokalemia
Clinical findings Potassium is an electrolyte present in all body fluids but concentrated
inside cells, where it helps regulate water and acid-base balance, par
-
ticipates in nerve conduction, and stimulates contraction of muscle
cells. Along with calcium and magnesium, potassium controls cardiac
output (heart rate
dietary sources and excreted primarily through the kidneys. A serum
potassium level <3.5 mEq/L defines hypokalemia.
Diuretic drugs are the most common cause of potassium deficiency,
with the reduction being dose-dependent and usually mild. Other
conditions implicated in hypokalemia include chronic starvation,
prolonged IV hydration without potassium replacement, prolonged
vomiting or diarrhea, hyperaldosteronism, fluid loss from intestinal
fistula, excessive loss of potassium in urine, loss from draining
wounds, chronic heavy alcohol use, treatment of megaloblastic anemia
with vitamin B
12
or folate, and cystic fibrosis. Other medications asso-
ciated with hypokalemia include corticosteroids, β-adrenergic ago-
nists such as isoproterenol, β-adrenergic antagonists such as clonidine,
antibiotics such as gentamicin and carbenicillin, and the antifungal
agent amphotericin B.
Hypokalemia is often asymptomatic. Clinical signs and symptoms are
more likely in elderly patients, including the following:
•
Malaise, fatigue, lethargy
• Weakness, rhabdomyolysis
• Hyporeflexia
• Muscle cramps, myalgias
• Loss of appetite
• Increased thirst
• Urinary frequency or polyuria
• Vomiting, constipation
• Weak pulse
• Irregular heart rhythm
• Hypotension
• Delirium or confusion
Severe untreated hypokalemia can be fatal.
Laboratory testing Potassium levels at the low end of the normal range are usually asso-
ciated with potassium deficiency, as is a trend downward of as little as
0.1–0.2 mEq/day. Often, the cause is apparent (e.g., diuretic use). Lev
-
els below the reference range are stratified as follows:
• Mild: 3.1–3.5 mEq/L
• Moderate: 2.6–3.0 mEq/L
• Severe: ≤ 2.5 mEq/L
Diagnosis is more urgent and treatment algorithms more aggressive
for moderate to severe hypokalemia. For patients with an elevated risk
of cardiac dysrhythmias, even mild hypokalemia can be serious. These
include elderly patients, those with preexisting cardiac disease, those
receiving digoxin, and post-MI patients. In the latter population, po-
tassium levels should be maintained at ≥4.0 mEq/L.
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448 Laboratory Medicine in Psychiatry and Behavioral Science
Hypokalemia (continued)
Laboratory testing
(continued)
The following laboratory tests are recommended in the workup for
hypokalemia:
• ECG
• Serum potassium (recheck)
• Serum magnesium
• Serum glucose
• Urine electrolytes, urine creatinine (urine potassium–to-creatinine
ratio >1.5 mEq/mmol suggests urinary potassium wasting)
• Arterial blood gas to evaluate acid-base balance
If no cause is identified, further workup would include thyroid and
adrenal function testing.
ECG changes of hypokalemia include the following:
• Flattened T waves
• ST interval depression
• T wave inversion
• PR interval prolongation
• Appearance of U waves, with increasing amplitude
• Premature atrial contractions
• Prolonged QTc interval
• Premature ventricular contractions
• Ventricular tachycardia
• Torsades de pointes
• Ventricular fibrillation (K
+
<2 mEq/L)
Alfano G, Ferrari A, Fontana F, et al: Hypokalemia in patients with COVID-19. Clin Exp Nephrol
25(4):401–409, 2021
Ballantyne F III, Vander Ark C: The difficult diagnosis of hypokalemia. Am Fam Physician 33:256–258, 1986
Elliott TL, Braun M: Electrolytes: potassium disorders.FP Essent 459:21–28, 2017
Viera AJ, Wouk N: Potassium disorders: hypokalemia and hyperkalemia.Am Fam Physician 92(6):487–
495, 2015
Wang X, Han D, Li
48(1):300060518811058, 2020
https://t.me/med1917
449 Diseases and Conditions
Hypomagnesemia
Clinical findings Magnesium is an essential nutrient that serves as a cofactor for hun-
dreds of enzymatic processes involved in DNA replication, bone for-
mation, blood sugar regulation, blood pressure control, and heart,
nerve, and muscle function. An adequate level of magnesium is main
-
tained primarily via its reabsorption in the kidney. Risk factors for hy-
pomagnesemia include advanced age, inadequate dietary intake,
alcohol use disorder, significant diarrhea, malabsorption in the small
intestine, the presence of type 2 diabetes mellitus, and the use of med
-
ic ations su ch a s proton pump inhibitors, diuretics, antibiotics, bisphos-
phonates, certain monoclonal antibodies (e.g., denosumab), and
antineoplastics. In addition, more than a dozen genetic mutations as
-
sociated with renal magnesium wasting have been described.
Signs and symptoms of magnesium deficiency include the following:
• Fatigue, weakness
• Poor appetite
• Nausea, vomiting
• Cardiac rate and rhythm disturbances
• Neuromuscular irritability (e.g., cramps, tetany)
• Paresthesias
• Seizures
• Delirium
Consequences of hypomagnesemia include the following:
• Hypertension
•
ECG changes: widened QRS, prolonged PR, prolonged QT, tall
peaked T waves or inverted T waves, U waves
•
Arrhythmias: supraventricular tachycardia, ventricular arrhyth-
mias, torsades de pointes
•
Sudden cardiac death
• Risk of digitalis toxicity
• Impaired release of and skeletal resistance to PTH
• Vertigo, ataxia
• Depression, psychosis
•
Other electrolyte disorders: hypokalemia, hypocalcemia, hypo-
phosphatemia
Low magnesium also significantly increases morbidity in patients with
comorbid diseases such as type 2 diabetes who exhibit a more rapid
progression of disease and a higher risk of diabetic complications. Pa-
tients with primary hyperparathyroidism who become magnesium
deficient not only have more severe disease but also have a higher risk
of osteoporosis, anemia, and hypercalcemic crisis. Because magnesium
modulates vasomotor tone, blood pressure, and peripheral blood flow,
deficiency can have significant cardiovascular effects, including wors-
ening hypertension, onset of cardiovascular disease, and the appear-
https://t.me/med1917
450 Laboratory Medicine in Psychiatry and Behavioral Science
Hypomagnesemia (continued)
Laboratory testing Magnesium is sometimes overlooked as a cause of presenting symp-
toms because it is not part of the BMP or CMP. The magnesium level
should be checked when unexplained hypocalcemia or hypokalemia
is noted, in the presence of a ventricular arrhythmia, when drugs
implicated in hypomagnesemia are administered, or when any other
risk factor is present.
Magnesium levels <1.6 mg/dL are common. Clinical symptoms do not
usually appear until the level is <1.2 mg/dL. Analogous to the situ
-
ation with calcium, a spurious result for magnesium can be obtained
when hypoalbuminemia is present, such that a published correction
formula should be used.
Bosman W, Hoenderop JGJ, de Baaij JHF: Genetic and drug-induced hypomagnesemia: different cause,
same mechanism.Proc Nutr Soc 80(3):327–338, 2021
Chrysant SG, Chrysant GS: Adverse cardiovascular and blood pressure effects of drug-induced hypo-
magnesemia. Expert Opin Drug Saf 19(1):59–67, 2020
Na D, Tao G, Shu-Ying L, et al: Association between hypomagnesemia and severity of primary hyper-
parathyroidism: a retrospective study. BMC Endocr Disord 21(1):170, 2021
Srinutta T, Chewcharat A, Takkavatakarn K, et al: Proton pump inhibitors and hypomagnesemia: a meta-
analysis of observational studies.Medicine (Baltimore) 98(44):e17788, 2019
van Kempen TATG, Deixler E: SARS-CoV-2: influence of phosphate and magnesium, moderated by vita-
min D, on energy (ATP) metabolism and on severity of COVID-19.Am J Physiol Endocrinol Metab
320(1):E2-E6, 2021
Viering DHHM, de Baaij JHF, Walsh SB, et al: Genetic causes of hypomagnesemia, a clinical overview.Pe-
diatr Nephrol 32(7):1123–1135, 2017
https://t.me/med1917
451 Diseases and Conditions
Hyponatremia
Clinical findings Hyponatremia is defined by a serum sodium level <136 mEq/L, re-
flecting excess water relative to sodium. In this situation, water shifts
into cells, causing them to swell and giving rise to a range of primarily
neuropsychiatric symptoms, including the following:
• Lethargy
• Weakness
• Restlessness
• Headache
• Disorientation
• Delirium, confusion
• Nausea, vomiting
• Muscle cramps
• Myoclonus
• Asterixis
• Seizures
• Papilledema
• Coma and death
Hyponatremia is associated with several conditions encountered in
psychiatric practice, including psychogenic polydipsia, SIAD, beer
potomania, postsurgical pain, and use of drugs of abuse such as
amphetamines, Ecstasy, and bath salts, as well as a long list of psycho
-
tropic drugs (especially antipsychotics and antidepressants). Common
causes in the general medical population include use of diuretics, diar
-
rhea, heart failure, liver disease, and kidney disease. In elderly patients,
adrenal insufficiency secondary to pituitary disease should be consid-
ered. See also the discussion in the Sodium entry in the Laboratory
Tests chapter for further details.
Laboratory testing The lower limit of normal for sodium is 136 mEq/L in adults
(132 mEq/L in those older than 90 years). The critical value for hypo-
natremia is <120 mEq/L, for which urgent intervention is required.
Other tests used in the initial workup of hyponatremia include serum
osmolality, urine osmolality, and urine sodium. In compulsive water
drinking, psychogenic polydipsia (associated with schizophrenia), or
beer potomania (in heavy beer drinkers), serum sodium, serum osmo
-
lality, and urine osmolality are all low. In SIAD, serum sodium and
serum osmolality are low, but urine osmolality is not low.
Adrogue HJ, Madias NE: Hyponatremia. N Engl J Med 342:1581–1589, 2000
Braun MM, Barstow CH, Pyzocha NJ: Diagnosis and management of sodium disorders: hyponatremia
and hypernatremia. Am Fam Physician 91(5):299–307, 2015
Buffington MA, Abreo K: Hyponatremia: a review. J Intensive Care Med 31(4):223–236, 2016
Hoorn EJ, Zietse R: Diagnosis and treatment of hyponatremia: compilation of the guidelines.J Am Soc
Nephrol 28(5):1340–1349, 2017
Kugler JP, Hustead T: Hyponatremia and hypernatremia in the elderly. Am Fam Physician 61:3623–3630,
2000
Lien YH, Shapiro JI: Hyponatremia: clinical diagnosis and management. Am J Med 120:653–658, 2007
Palmer BF, Clegg DJ: Electrolyte disturbances in patients with chronic alcohol-use disorder.N Engl J Med
377(14):1368–1377, 2017
Sterns RH: Disorders of plasma sodium: causes, consequences, and correction.N Engl J Med 372(1):55–
65, 2015
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