45. HYPERTENSION 217 5. Enalaprilat. Effective in 5–10 mcg/kg doses q8–24h. Because neonates have a more active renin-angiotensin system, they are more sensitive to drug than older children and should be given dose in lower range. Closely monitor renal function and serum potassium level. 6. Hydralazine. Old but trustworthy drug given at 0.1–0.5 mg/kg as a bolus. Maximum dose per bolus is 20 mg. Can be repeat- ed q3–4h. Monitor heart rate and hold doses if significant tachycardia. Watch for resistance to BP-lowering effect. 7. Diazoxide. Extremely effective; can cause precipitous drop in BP and elevate blood glucose concentration. If normal saline infusion is available at bedside to treat acute hypotension, 1–3 mg/kg quick IV push works well. Second bolus can be given within 5–15 minutes if needed, not to exceed 5 mg/kg com- bined dose. Effective dose can be repeated q4–24h. B. Hypertensive Urgency. Symptomatic hypertension without evi- dence of end-organ damage. Oral treatment is acceptable, although IV medications may also be considered. Long-acting oral agents (ie, those recommended in once- or twice-daily doses) should be avoided due to delayed peak concentration. 1. “Sublingual” nifedipine. No excessive side effects reported in pediatric literature; frequently administered, convenient drug of choice for pediatric hypertensive urgencies if administered in appropriate dose. Conventional dose is 0.25–0.5 mg/kg per dose q3–4h, not to exceed 10 mg per dose or 3 mg/kg/day. Although labeled as sublingual, absorption takes place from stomach, so capsule needs to be opened before being swal- lowing. 2. Oral hydralazine. Doses of 0.75–1 mg/kg q4–6h may work well. Maximum one-time dose is 25 mg, with cumulative daily dose of 5 mg/kg. 3. Minoxidil. More powerful vasodilator than hydralazine, with more side effects. In acute situations, 0.2 mg/kg may work well. Add diuretic if treatment exceeds a few days. 4. Propranolol. Given in doses of 0.12–0.25 mg/kg q6–12h. 5. Chronic hypertension. Not within scope of this discussion, but lifestyle changes, such as low-salt diet, exercise, and weight loss, should be part of any comprehensive treatment plan for patients with chronic hypertension. VI. Problem Case Diagnosis. The 13-year-old girl had modest BP elevation, which might be attributed to office hypertension, essen- tial hypertension, or metabolic syndrome. Further investigation showed multiple high BP readings had been obtained by school nurse, and patient also had a strong family history of hypertension. Diagnosis of essential hypertension was made, and patient’s BP was well controlled on salt restriction and hydrochlorothiazide, 25 mg daily. 218 I: ON CALL PROBLEMS VII. Teaching Pearl: Question. What is the only form of hypertension that will never develop into malignant hypertension? VIII. Teaching Pearl: Answer. Coarctation of the aorta never progresses into malignant hypertension. This is the only form of hypertension in which the kidneys are sheltered from elevated systemic BP. This observation suggests the pivotal role of the kidneys in the pathome- chanism of malignant hypertension. REFERENCES Fivush B, Neu AM, Furth S. Acute hypertensive crises in children: Emergencies and urgencies. Curr Opin Pediatr 1997;9:233–236. Friedman AL. Approach to the treatment of hypertension in children. Heart Dis 2002;4:47–50. National High Blood Pressure Education Working Group on Hypertension Control in Children and Adolescents. Update on the 1987 task force report on high blood pressure in children and adolescents: A working group report from the National High Blood Pressure Education Program. Pediatrics 1996;98:649–658. Sinaiko AR. Hypertension in children. N Engl J Med 1996;335:1968–1973. 46. HYPOCALCEMIA I. Problem. A 7-day-old infant is admitted with a history of jitteriness and poor feeding associated with total serum calcium level of 6.0 mg/dL (normal for this age: 7.6–10.9 mg/dL). II. Immediate Questions A. Is patient symptomatic? Hypocalcemia can be asymptomatic or associated with serious life-threatening manifestations. Severe manifestations that require immediate treatment include pares- thesias, tetany, laryngospasm, and seizures. Diagnostic signs suggesting the need for immediate treatment are positive Chvostek and Trousseau signs. B. Is low serum calcium level an artifact or reflective of low ion- ized calcium? Whereas total serum calcium is routinely meas- ured, it is the ionized calcium component that is physiologically important. Ionized calcium can be measured directly or can be estimated by subtracting 0.8 mg/dL for every 1 g/dL by which serum albumin is < 4 g/dL. C. Is serum magnesium level low? Serum calcium will not respond to correction with IV or oral calcium as long as severe hypomag- nesemia remains untreated. D. Pertinent Historical Information 1. Infants. Is there a history of parathyroid or other endocrine dis- eases? What is the gestational history? Pay particular attention to maternal illnesses (eg, diabetes mellitus, hyperparathy- roidism), medications, birth history, and gestational age. What type of formula or supplements is infant given? 46. HYPOCALCEMIA 219 2. Children. Is there a history of acute or chronic illnesses, med- ication use, or surgery? Ask about diet and sun exposure. III. Differential Diagnosis. Causes of hypocalcemia in infants need to be distinguished from those in children. Neonatal hypocalcemia is classically divided into early (first 4 days of life) and late, which usu- ally presents at 5–10 days of life. In children of all ages, abnormali- ties can be divided into those involving parathyroid hormone (PTH), vitamin D, and binding or distribution of calcium. A. Neonatal Hypocalcemia 1. Early neonatal hypocalcemia a. Preterm infants. Transiently decreased PTH secretion. b. Neonates with asphyxia. Possibly associated with increased calcitonin secretion. c. Infants of diabetic mothers. Related to maternal hypo- magnesemia. d. Infants whose mothers had preeclampsia. Related to maternal hypomagnesemia. 2. Late neonatal hypocalcemia a. Dietary phosphate loading. Results from inability of imma- ture kidneys to excrete phosphate in infants fed cow’s milk formula. b. Hypoparathyroidism. Transient, insufficient PTH secretion. c. Hypomagnesemia. Can be associated with rare defects in magnesium transport. 3. Miscellaneous causes of hypocalcemia in infants and neonates a. Congenital hypoparathyroidism. Can be associated with DiGeorge anomaly or CATCH-22 syndrome (cardiac anom- alies, abnormal facies, thymic aplasia, cleft palate, hypocal- cemia, caused by deletion in chromosome 22q11.2). b. “Late-late” hypocalcemia. Skeletal hypomineralization and poor mineral and vitamin D intake presenting at 2–4 months of age. c. Infants of hyperparathyroid mothers. d. Ionized hypocalcemia. Associated with exchange trans- fusions of citrated blood, lipid infusions, or respiratory alkalosis. B. Childhood Hypocalcemia 1. Parathyroid disorders a. Hypoparathyroidism. Associated with chromosome 22q11 abnormalities (see A, 3, a, earlier) or autoimmune syn- dromes such as autoimmune polyglandular syndrome. b. Pseudohypoparathyroidism. Disorders of activation of the cellular effects of PTH. c. Calcium-sensing abnormalities. Occurs when parathy- roid gland is abnormally sensitive to serum calcium, causing PTH levels to be low in relation to level of calcium. 220 I: ON CALL PROBLEMS d. Hypomagnesemia. Associated with decreased PTH secre- tion and PTH effect. 2. Vitamin D disorders a. Vitamin D deficiency. Low levels of vitamin D due to dietary insufficiency, lack of sunshine, fat malabsorption, or liver disease. b. Vitamin D–dependent rickets. Block in 1,25-dihydroxyvitamin D formation (type 1) or abnormal receptor (type 2). c. Renal failure. Acute or chronic, with inadequate formation of 1,25-dihydroxyvitamin D. d. Fanconi syndrome. Proximal renal tubular dysfunction with low 1,25-dihydroxyvitamin D formation and renal phosphate wasting. e. Altered metabolism. Often due to drugs such as pheno- barbital, phenytoin, or ketoconazole. 3. Abnormal distribution or binding of calcium a. Tumor lysis syndrome. Hyperphosphatemia, hypocalcemia, and acute renal failure. b. Acute rhabdomyolysis. Trapping of calcium into injured muscle. c. Hungry bone syndrome. Shift of calcium and phosphorus into bone, often after parathyroidectomy. d. Drugs. Foscarnet, bisphosphonates, calcitonin, calcium chelators (citrate, phosphorus). e. Miscellaneous. Acute pancreatitis, toxic shock syndrome, sepsis. IV. Database A. Physical Exam Key Points 1. General appearance. Albright hereditary osteodystrophy with pseudohypoparathyroidism (short stature, obesity, round face); large-for-gestational-age infants of diabetic mothers. 2. Skin. Mucocutaneous candidiasis with autoimmune polyglandular syndrome; alopecia with type 2 vitamin D–dependent rickets. 3. HEENT. Facial features of DiGeorge syndrome, laryngospasm, cataracts. 4. Skeletal findings. Evidence of bowing with rickets; short metacarpals and metatarsals with pseudohypoparathyroidism. 5. Neuromuscular exam. Neuromuscular excitability manifested by irritability, facial grimacing, hyperactive deep tendon reflexes, muscular spasms, twitching and tetany, confusion, seizures. 6. Heart. Cardiac abnormalities seen in DiGeorge syndrome. 7. Specific tests for tetany of hypocalcemia a. Chvostek sign. Elicited by tapping on the facial nerve below the zygomatic arch and 2 cm anterior to the earlobe. Positive sign ranges from twitching of the lip at the angle of the mouth to contraction of the facial muscles. 46. HYPOCALCEMIA 221 b. Trousseau sign. Performed by inflating a BP cuff on the upper arm to just above systolic BP for 3 minutes. With hypocalcemia, carpal spasm may occur in response to ischemia of the ulnar nerve. B. Laboratory Data 1. Serum electrolytes. In addition to total calcium, focus on potassium, phosphate, and magnesium levels. The latter two are not usually included in standard panels and may have to be ordered separately. Serum calcium should be interpreted in relation to serum albumin (see II, B, earlier). Hyperkalemia may be a sign of tumor lysis. Serum phosphate is elevated in renal failure, tumor lysis, rhabdomyolysis, phosphate enemas, and parathyroid disorders. It is also seen in most of the neonatal hypocalcemic disorders. Hypophosphatemia is a sign of vitamin D disorders, hungry bone syndrome, and Fanconi syndrome. Severe hypomagnesemia, < 1 mg/dL, is a cause of refractory hypocalcemia. 2. Serum albumin. As previously described. 3. Ionized calcium. Particularly valuable in the presence of alkalosis and chelators, which may selectively lower ionized calcium. In confusing cases, ionized calcium can help with diagnosis and management. 4. BUN and creatinine. Signs of renal failure, acute or chronic. 5. PTH level. Should be interpreted in relation to serum calcium level. 6. Vitamin D levels. 25-Hydroxyvitamin D identifies deficiency or abnormalities of metabolism whereas 1,25-dihydroxyvitamin D may be helpful in patients with vitamin D–dependent states and renal disease. C. Radiographic and Other Studies 1. Bone films. Look for rickets, osteopenia, or renal osteody- strophy. 2. ECG. Hypocalcemia may result in prolonged QT interval or T wave inversion. V. Plan. Evaluate for symptomatic hypocalcemia that would necessitate immediate IV treatment with calcium and possibly magnesium. Obtain laboratory studies and initiate oral treatment after patient is stabilized. A. Neonates 1. Emergency treatment a. For symptomatic hypocalcemia or when serum calcium is < 5–6 mg/dL, give 10–20 mg elemental calcium per kilogram body weight, or 1–2 mL of calcium gluconate per kilogram body weight (10% solution). This should be given no faster than 1 mL/min under constant cardiac monitoring. b. Treat hypomagnesemia with 0.1–0.2 mL/kg of 50% magne- sium sulfate (0.4–0.8 mEq/kg or 5–10 mg/kg) IV or IM, again 222 I: ON CALL PROBLEMS under constant cardiac monitoring. May repeat magnesium dose q12–24h. 2. Nonemergency or maintenance therapy. Oral calcium at a dose of 50–75 mg elemental calcium per kilogram per day as cal- cium glubionate (23 mg/mL), calcium carbonate (100 mg/mL), or calcium gluconate (9 mg/mL). Give in 4–6 divided doses, and combine with low-phosphorus formula such as maternal breast milk or Similac PM 60/40. 3. Vitamin D. Daily supplement of oral vitamin D at a dose of 400–2000 IU/day. B. Children 1. Emergency treatment a. For acute symptomatic hypocalcemia, give 2–3 mg elemen- tal calcium per kilogram body weight or 0.25 mL calcium gluconate per kilogram body weight (10% solution) IV at a rate of no more than 1 mL/min under constant cardiac mon- itoring. Can continue with a constant infusion at a rate of 50–75 mg elemental calcium per kilogram per day until hypocalcemia is corrected. b. For hypomagnesemic hypocalcemia, give 6 mg elemental magnesium per kilogram body weight or 0.12 mL per kilo- gram body weight of 50% magnesium sulfate IM or IV over 1–4 hours. 2. Chronic treatment a. Calcium. Oral calcium at a dose of 500–1000 mg elemental calcium per dose q6h. This can be given as liquid (calcium carbonate, 100 mg/mL; calcium glubionate, 25 mg/mL) or one of many tablet forms. b. Vitamin D. Treat vitamin D deficiency with ergocalciferol drops at a dose of 800–8000 IU/day. Doses have been described in the literature up to 600,000 units given in a single day. For patients with renal failure, calcitriol can be given at a dose of 0.25–1 mcg/day. Patients with hypoparathyroidism, pseudohypoparathyroidism, and vita- min D–dependent rickets type 1 also require calcitriol thera- py rather than ergocalciferol. This can be given orally or intravenously. VI. Problem Case Diagnosis. The 1-week-old infant had late neonatal hypocalcemia, and a phosphorus level of 9.2 mg/dL. Infant was treated with IV calcium gluconate and placed on Similac PM 60/40. There was no evidence of DiGeorge syndrome or recurrence of hypocalcemia. VII. Teaching Pearl: Question. In most cases of vitamin D–deficiency rickets, is the level of 1,25-dihydroxyvitamin D high, normal, or low? VIII. Teaching Pearl: Answer. The 1,25-dihydroxyvitamin D levels are usually in the normal range, but this is inappropriate for the level of 47. HYPOGLYCEMIA 223 hypophosphatemia, hypocalcemia, and hyperparathyroidism that may be present. REFERENCES Carpenter TO. Neonatal hypocalcemia. In: Favus M, ed. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 5th ed. American Society of Bone and Mineral Research, 2003:286–288. Koo W. Hypocalcemia and hypercalcemia in neonates. In: Umpaichitra V, Bastian W, Castells S. Hypocalcemia in children: Pathogenesis and management. Clin Pediatr 2001;40:305. 47. HYPOGLYCEMIA I. Problem. A previously healthy 3-year-old boy is brought to the emer- gency department in the early morning after his parents found him difficult to arouse. The family had been traveling and the child had a prolonged fast. His blood glucose level is 28 mg/dL. II. Immediate Questions A. What constitutes a low serum glucose level in a patient of this age? Hypoglycemia in children is defined as follows. 1. Term neonate. Serum glucose < 50–60 mg/dL. 2. Infants and young children. Serum glucose < 45–60 mg/dL. 3. Older children and adolescents. Serum glucose < 60 mg/dL. B. What is patient’s mental status? An unconscious patient must first be stabilized. Quickly assess ABCs (airway, breathing, and circulation) and obtain access to draw samples for laboratory analysis and provide glucose. C. Is patient diabetic? Excess insulin administration or administra- tion of insulin in a patient who is not eating can induce hypo- glycemia. D. Has patient had adequate intake? Was TPN abruptly discon- tinued? Often children who are sick have decreased oral intake and may not have had anything to eat or drink for several hours. Abrupt discontinuation of dextrose-containing fluids can also lead to hypoglycemia. E. Is ingestion a possibility? Many different agents can induce hypoglycemia, including salicylates, alcohol, and oral hypo- glycemic agents. F. Is patient a newborn, an infant of a diabetic mother, intrauter- ine growth retarded (IUGR), or small or large for gestational age (SGA or LGA)? Infants of diabetic mothers are often hyperin- sulinemic at birth and when glucose stores from the placenta are removed can become hypoglycemic. SGA infants (defined as < 10th percentile or < 2.5 kg at term) and LGA infants (defined as > 95th percentile or > 4.0 kg at term) are at increased risk of hypoglycemia. G. What symptoms are associated with hypoglycemia? Symptoms include anxiety, diaphoresis, jitteriness, weakness, 224 I: ON CALL PROBLEMS nausea, headache, and confusion. Infants with hypoglycemia can present with few symptoms. III. Differential Diagnosis A. Medications 1. Insulin. Check for administration error, including patient identi- ty, dose, preparation, and route. 2. Other medications. Ingestion of agents such as oral hypo- glycemics, salicylates, quinine, and pentamidine can lead to hypoglycemia. 3. Ethanol. Consider accidental ingestion of alcohol or other ethanol-containing substances such as mouthwash. B. Inborn Errors of Metabolism 1. Carbohydrate metabolism. Examples include galactosemia and glycogen storage diseases. 2. Lipid metabolism. Examples include carnitine deficiencies; very long–, long-, medium-, and short-chain acyl-CoA dehy- drogenase deficiency. 3. Amino acid metabolism. Examples include Maple syrup urine disease and methylmalonic acidemia. C. Neonatal Causes 1. Gestational diabetes. These infants, often LGA, are hyperin- sulinemic at birth and can become hypoglycemic when the pla- cental glucose source is removed. 2. IUGR or SGA. These infants can have limited glycogen stores and decreased body fat and muscle protein. 3. Perinatal stress. Stressors such as fetal hypoxia and prema- turity can lead to hypoglycemia. 4. Genetic malformations. Patients with Beckwith-Wiedemann syndrome may exhibit hypoglycemia. D. Ketotic Hypoglycemia. This is the most common form of child- hood hypoglycemia and is related to prolonged fast, usually with intercurrent illness. Typical presentation is a child, aged 18 months to 5 years, who has missed dinner or breakfast and is found to be difficult to arouse. Can be associated with seizures and lead to coma. E. Sepsis. Hypoglycemia or hyperglycemia can occur in septic shock. Usually a sign of late infection. F. Severe Liver Failure. Glycogen stores are easily depleted in patients with advanced liver disease and destruction. G. Reactive Hypoglycemia. Can occur post-prandially in a small percentage of the population, especially in patients with dumping syndrome. H. Endocrinopathies. Includes adrenal insufficiency, hypothy- roidism, and hypopituitarism. I. Abrupt Discontinuation of TPN. Rare. 47. HYPOGLYCEMIA 225 J. Factitious Hypoglycemia. Due to laboratory error (unspun blood that sits out too long) or as a result of leukocyte metabolism in a patient with markedly increased WBC count. K. Insulinoma or Other Neoplasms. L. Other Causes. Severe malnutrition, seizures, vasovagal fainting, narcolepsy, and anxiety attack. IV. Database A. Physical Exam Key Points 1. Assess airway, breathing, and circulation (ABCs) and vital signs. 2. Evaluate for hepatomegaly, pigmentation, short stature, and neurologic signs. B. Laboratory Data. Careful history and physical exam usually pro- vide clues to diagnosis. Patients with a history of hypoglycemia may require hospital admission to induce hypoglycemia and to obtain laboratory data during an acute episode. 1. Obtain serum glucose, insulin, cortisol, and growth hormone levels, and urinalysis for ketones. If possible, also obtain C-peptide, lactate, ammonia, thyroid-stimulating hormone, and thyroxine levels. 2. Serum electrolytes, renal and liver function studies, and CBC may be helpful in evaluating some of the causes listed under differential diagnosis, earlier. C. Radiographic and Other Studies. May be indicated to evaluate for insulinoma, malignancy, and pituitary lesions if suggested by history, physical exam, or screening studies. V. Plan A. Administer Glucose. If hypoglycemia is strongly suspected, do not wait for results of serum glucose testing. 1. Oral. Preferred initial therapy if patient is awake and has an intact airway. Give orange juice by mouth or via nasogastric (NG) or orogastric (OG) tube. 2. Parenteral. In children, give a 2 mL/kg bolus of D 25 W IV or IO. In infants, give a 2–4 mL/kg bolus of D 10 W IV or IO. After the dextrose bolus, patient should be started on mainte- nance D 10 W electrolyte solution to provide glucose at a rate of 6–8 mg/kg/min. 3. Intramuscular or subcutaneous (IM or SQ). If no IV access is available, give glucagon IM or SQ. a. Neonate. Dose is 0.3 mg/kg IM or SQ. b. Child or adolescent. Dose is 0.5–1 mg IM or SQ. 4. Other agents. Diazoxide, octreotide, and hydrocortisone may have a role in treatment of hypoglycemia, depending on the cause. [...]... admitted after several days of poor oral intake and significant vomiting and diarrhea During a physical exam, she develops a tonic-clonic seizure Laboratory values show serum sodium concentration of 1 14 mEq/L (normal: 136– 146 mEq/L) II Immediate Questions A Is patient adequately ventilated, with a safe and patent airway? It is critical to assess the ABCs (airway, breathing, and circulation) because hyponatremia... (hypocalcemia) 2 ABGs Remember, alkalosis can cause intracellular shift of potassium In addition, many of the renal causes of potassium 228 I: ON CALL PROBLEMS loss have an associated acid-base disturbance Finally, an anion gap acidosis may be present in the setting of elevated lactate with severe dehydration, poor cardiac output, or sepsis Treatment of acidosis produces a “relative alkalosis” and may exacerbate... Subramanian R, Khardori R Severe hypophosphatemia: Pathophysiologic implications, clinical presentations, and treatment Medicine 2000;79:1  240 I: ON CALL PROBLEMS 52 HYPOTENSION I Problem A 2-year-old boy who was admitted earlier in the day with diarrhea and dehydration now has a BP of 64/ 33 II Immediate Questions A What are the vital signs? Is patient adequately perfused? Are airway, breathing, and... resuscitation if appropriate C Cardiac Dysfunction Although uncommon in pediatric patients, myocarditis may present with hypotension and sinus tachycardia Likewise, pericarditis with pericardial effusion and cardiac tamponade may present in a similar fashion Finally, consider other things that may impair cardiac output: tension pneumothorax, high positive end-expiratory pressure if mechanically ventilated... redistribution, renal loss, GI loss, other loss (sweating), or inadequate intake A Redistribution Hypokalemia Potassium is primarily an intracellular ion; hence a small shift of this ion into the cell can cause a 48 HYPOKALEMIA B C D E 227 large change in plasma potassium concentration Extracellular potassium can shift into the intracellular space in the setting of alkalosis, ␤-agonist use, catecholamine... cerebral atrophy, or congenital malformation 4 Chest x-ray If respiratory symptoms are present V Plan Most children with hypotonia have a chronic or subacute presentation It is critical to recognize an acute presentation of hypotonia Thorough history and physical exam allow clinician to narrow the differential diagnosis based on its chronicity and anatomic classification This in turn allows for systematic... what are fluid orders? Confirm that appropriate IV solutions are being administered 3 Does past history include any factors that could influence homeostatic mechanisms for water and salt balance? Medications (eg, diuretics) and disorders such as renal failure, heart failure, ascites, and intracranial masses may alter the body’s normal water and salt control mechanisms III Differential Diagnosis Hyponatremia... hypokalemia and alkalosis 6 Postrenal transplantation In addition to cyclosporine A 7 Diabetes mellitus IV Database A Physical Exam Key Point 1 Cardiovascular Irregular heartbeat and hypertension 2 Neuromuscular Check for neuromuscular excitability with Chvostek and Trousseau signs (see Chapter 46 , Hypocalcemia, IV, A, 7, p 220) Muscular tremor, weakness, and carpopedal spasm may be present Observe for ataxia,... x-ray Look for pulmonary edema or aspiration 2 Continuous ECG monitoring Rule out cardiac dysrhythmia 3 CT scan Used to rule out intracranial or intra-abdominal process, especially in suspected trauma patients 4 Neck x-rays Often needed in patients with suspected head or neck trauma to evaluate the cervical spine V Plan Management must address the underlying condition impairing thermoregulation that... post– renal transplantation status 2 Hyperparathyroidism Primary (rare in children) or secondary to vitamin D deficiency or other nonrenal causes 3 Diuretic phase of acute tubular necrosis (ATN) 4 Postobstructive diuresis 5 Post–renal transplantation status C Increased GI Losses 1 Use of oral phosphate-binding antacids 2 Decreased intake Starvation, anorexia nervosa, proteincalorie malnutrition At high . and neonates a. Congenital hypoparathyroidism. Can be associated with DiGeorge anomaly or CATCH-22 syndrome (cardiac anom- alies, abnormal facies, thymic aplasia, cleft palate, hypocal- cemia,. seizures, vasovagal fainting, narcolepsy, and anxiety attack. IV. Database A. Physical Exam Key Points 1. Assess airway, breathing, and circulation (ABCs) and vital signs. 2. Evaluate for hepatomegaly,. is primarily an intracel- lular ion; hence a small shift of this ion into the cell can cause a 48 . HYPOKALEMIA 227 large change in plasma potassium concentration. Extracellular potassium can shift