Week 18: Petrifying pH and Spooooooky Electrolytes

Acidosis and alkalosis are processes that lead to acidemia (pH < 7.40) and alkalemia (pH > 7.40). Primary metabolic disorders result from a change in bicarbonate, while primary respiratory disorders result from a change in partial pressure of carbon dioxide. Compensation occurs when other system alterations bring the blood gas toward a normal pH of 7.35. A metabolic acidosis is present in any patient with a pH of < 7.35 and bicarbonate < 24. Causes of an increased anion gap acidosis [Na+ – (Cl- + HCO3-)] > 12 can be remembered by the MUDPILES mnemonic (Methanol, Metformin, Uremia, Diabetic (or alcoholic) ketoacidosis, Paraldehyde, Propylene glycol, Isoniazid, Iron, Lactic acidosis, Ethylene glycol, Salicylates). Normal anion gap acidosis is caused by: renal losses (tubular acidosis, acetazolamide), GI losses (diarrhea, malabsorption), and adrenal insufficiency. Compensation for an acid-base disorder never completely normalizes the pH. A pH of 7.45 in a patient with low bicarbonate indicates a second disorder (such as a primary respiratory alkalosis).

Metabolic alkalosis (B) is caused by an increase in bicarbonate leading to a pH > 7.35. This occurs secondary to gastric acid loss from vomiting or NG tube suctioning, diuretic use, and adrenocortical hormone excess. Respiratory acidosis (C) is caused by an increase in the partial pressure of carbon dioxide > 40 leading to a pH < 7.35. This is primarily a result of inadequate ventilation or increased dead space. Causes include head or chest trauma, oversedation, obtundation, neuromuscular disorders, Pickwickian syndrome (obesity-hypoventilation syndrome), and COPD. Respiratory alkalosis (D) is caused by a decrease in the partial pressure of carbon dioxide < 40 leading to a pH > 7.35. In this condition, carbon dioxide ventilation outpaces production.

The patient has a likely pseudo-obstruction (ogilvie’s syndrome). While we would want to get CT imaging to rule out mechanical obstruction, a pseudo-obstruction can occur in the elderly/nursing home patients. It’s cause is unknown, but is due to gut motility dysfunction.  Dehydration and associated hypokalemia are common. Hypokalemia can cause weakness of muscles, and when low can lend to gut motility dysfunction. Treatment measures include IV hydration, potassium repletion, nasogastric tube placement, and surgical consultation.

Hypercalcemia (A) can occur with malignancy, hyperparathyroidism, drugs, immobilization, Paget’s disease, or excessive intake (vitamin D toxicity, milk-alkali syndrome). Major clinical findings can be remembered with the phrase “stones, bones, groans, and psychiatric overtones” (nephrolithiasis, weakness, abdominal pain/constipation, confusion/depression). Hypercalcemia shortens the QT interval. Hypocalcemia (B) can be seen in renal failure, hypoparathyroidism, pancreatitis, or chronic malabsorption syndromes. Neurologic symptoms include paraesthesias, carpopedal spasm, Chvostek’s or Trousseau’s sign, and hyperreflexia. Cardiovascular signs include hypotension, heart failure, dysrhythmias, and prolonged QT interval. Hyperkalemia is more commonly seen in renal failure patients, and would be expected to primarily cause cardiac arrhythmias.

Hyponatremia is defined as sodium less than 135 mEq/L. Hyponatremia can occur in a hypovolemic, euvolemic, or hypervolemic state. Hypervolemic hypo-osmolar hyponatremia is is associated with fluid overload. The etiology is usually from a perceived low intravascular volume by the kidneys and active water reabsorbtion in excess to sodium retention. If urine sodium is low (<20) causes include liver failure, cirrhosis, hepatorenal syndrome, nephrotic syndrome, and CHF. If urine sodium is high (>20) causes include acute or chronic renal failure, such as that caused by hypertensive nephropathy. Treatment of hypervolemic hypo-osmolar hyponatremia is dialysis.

Cirrhosis (A) and congestive heart failure (B) is often the cause of hypervolemic hypo-osmolar hyponatremia when the urine sodium is low (<20). SIADH (D) results in euvolemic hyponatremia with urine osmolality greater than serum osmolality. The excess ADH causes total body water to increase thereby diluting total body sodium. Despite the increased total body water, these patients typically do not show evidence of edema or heart failure as the increased water is intracellular not intravascular.

This ECG is indicative of hyperkalemia, one of the most lethal complications of chronic kidney disease encountered in the ED. A potassium level of 6 mEq/L should be considered potentially dangerous, even though many patients with ESRD chronically tolerate serum levels above this and do not manifest ECG changes. The most rapid treatment for hyperkalemia is intravenous calcium (gluconate with peripheral access, chloride with central access), which transiently reverses cardiac effects of hyperkalemia by antagonism of potassium at the cardiac membrane. Calcium is indicated in all patients with suspected hyperkalemia who have widening of the QRS, an unstable dysrhythmia, bradycardia, or hypotension.

Cardiology consultation (B) is not needed; the patient’s ECG findings are due to an underlying electrolyte abnormality, not a primary cardiac condition. Defibrillation (C) may be necessary if the rhythm deteriorates to ventricular fibrillation. However, should that occur, the definitive management remains removal of potassium from the serum. Transcutaneous pacing (D) can be used as a temporizing measure in patients with symptomatic bradycardia. Hyperkalemic bradycardia responds poorly to pacing. The primary treatment is cardiac membrane stabilization with calcium and subsequent lowering of the serum potassium.

Hypokalemia frequently occurs concomitantly in patients with hypomagnesemia. Because magnesium is required for the normal functioning of the Na+/ K+ ATPase pump, as well as K+ reabsorption channels within the nephrons, hypomagnesemia can result in refractory hypokalemia that is not correctable by the administration of potassium alone. For potassium levels to increase, magnesium must also be administered.

Hypermagnesemia (A) enhances potassium retention. Hypernatremia (B) and hyponatremia (D) will not interfere with increasing the level of potassium in patients receiving potassium supplementation for hypokalemia.

D. Correct. Hyperventilation causes a respiratory alkalosis. This in turn increases serum pH and therefore enhances protein binding of calcium in serum. The end result is decreased free ionized calcium. This induced hypocalcemia causes muscle spasm and in severe cases may lead to a tetany like state

A. Incorrect. hyperventilation causes the opposite of the proposed mechanism

B. Incorrect. Increased PaO2 causes neuronal activation
Increased PaO2 is not the cause of carpal spasm

C. Incorrect. Increased serum pH causes vasodilation of capillary beds
Hyperventilation would not increase serum pH and is not the cause of carpal spasm

The syndrome of inappropriate secretion of ADH (SIADH) is defined by the secretion of ADH in the absence of an appropriate physiologic stimulus. Its hallmark is an inappropriately concentrated urine, despite the presence of a low serum osmolality and a normal circulating blood volume. Causes of SIADH include central nervous system disorders, pulmonary disease, drugs, stress, pain, and surgery. Therefore, the above patient, with a known history of lung cancer and hyponatremia, most likely has SIADH and exhibits the following lab findings: serum osmolarity low, urine osmolarity high, urine sodium high.

Psychogenic polydipsia (D) is a rare cause of euvolemic hyponatremia and is seen in psychiatric patients who consume large amounts of free water (in excess of 1 L/hr). This large consumption overwhelms the kidney’s ability to excrete free water. Patients will exhibit serum osmolarity low, urine osmolarity low, urine sodium low. Diabetes insipidus (B) results in the loss of large amounts of dilute urine from the loss of concentrating ability in the distal nephron. This may be due to a central cause—such as the lack of ADH secretion from the pituitary—or a nephrogenic cause—such as the lack of responsiveness to circulating ADH. Laboratory workup that invariably shows serum osmolarity high, urine osmolarity high, urine sodium low (A) rarely occurs.

The patient is in an acute metabolic acidosis as is evident by the pH and low bicarbonate. A quick calculation shows that the anion gap is 26 and that the respiratory response with a drop in PaCO2 to 22mmHg follows the “rule of 15’s” with the HCO3 of 8, displaying a proper hyperventilatory response to an acute metabolic acidosis and no evident mixed acid/base disorder. Anion gap is calculated by Na -HCO3 – Cl. For the rule of 15’s, HCO3 + 15 should = the pCO2 and the last 2 digits of the pH. In this patient, 8+15 = 23. This is the correct CO2 indicating an appropriate response. It is also the last 2 digits of the pH (7.23). Thus this is not a mixed acid base disorder but rather an acidosis with appropriate compensation. There are no ketones in the patient’s urine, and the lactate is elevated, thus this patient is in an acute lactic acidosis secondary to metformin rather than DKA.

A. Incorrect. Acute anion gap diabetic ketoacidosis
There are no ketones in the patient’s urine to suggest diabetic ketoacidosis.

C. Incorrect. Acute non-anion gap metabolic acidosis
This patient has an anion gap of 26 which is elevated and consistent with an anion gap acidosis. Recall anion gap is calculated by Na -HCO3 – Cl.

D. Incorrect. Mixed acid/base disorder
This patient has an appropriate compensatory response. Recall the rule of 15’s – HCO3 + 15 should = the pCO2 and the last 2 digits of the pH. In this patient, 8+15 = 23. This is the correct CO2 indicating an appropriate response. It is also the last 2 digits of the pH (7.23). Thus this is not a mixed acid base disorder but rather an acidosis with appropriate compensation. In addition if you apply the delta gap rule (AG-12/24-HCO3) you find that there is no underlying metabolic alkalosis. Recall that this rule tries to determine any underlying metabolic acidosis or alkalosis in an AGMA. if the gap <1: probable additional underlying metabolic acidosis, if it =1: pure AGMA, if it >1: additional underlying metabolic alkalosis

This patient presents with diabetic ketoacidosis as indicated by the laboratory findings of hyperglycemia, increased anion gap, acidemia, and low bicarbonate concentration. However, there is also a secondary primary metabolic acidosis present, likely caused by the patient’s diarrhea. The patient’s anion gap is increased by 8 mmol/L above the upper limit of normal of 12 mmol/L. In an isolated metabolic acidosis, the increase in anion gap correlates with the decrease in bicarbonate concentration (normal level is 24 mEq/L), and this difference is referred to as “delta gap” with normal values of 0 +/- 6. Thus, in this patient, the expected bicarbonate level would be 16 mEq/L +/- 6. However, the measured bicarbonate level is much lower than expected at 6 mEq/L. This indicates that a second non-anion gap metabolic acidosis is present. Diarrhea is a common cause of hyperchloremic (non-anion gap) metabolic acidosis.

This is a classic presentation of acute iron toxicity in a child. Iron exposure is one of the leading causes of poisoning deaths in children younger than six years. Iron is usually not considered poisonous and is often stored unsafely in many homes. It is easily accessible in prenatal vitamins and is often packaged as an appealing red sugar-coated tablet. Iron toxicity is associated with an anion-gap metabolic acidosis resulting primarily from increased lactate. Classic teaching describes five clinical stages of iron toxicity based on the pathophysiology of iron poisoning. Although conceptually important, they are of limited clinical benefit in managing the poisoned patient. Therefore, it is more clinically relevant to think about poisoning in two clinical stages. Nausea, vomiting, abdominal pain, and diarrhea characterize clinical stage one. The absence of symptoms, particularly vomiting, in the first six hours postingestion, excludes significant iron toxicity. Systemic toxicity is seen in clinical stage two, characterized by hepatotoxicity, coagulopathy, myocardial dysfunction, and neurologic symptoms, including seizures and altered mental status. Management is mainly supportive. Activated charcoal does not bind iron. Whole-bowel irrigation should be considered in a large ingestion. Intravenous deferoxamine is a chelating agent that should be considered in patients with severe iron toxicity. The PCO₂ should be decreased (A) as part of respiratory compensation, not increased. The patient should be acidemic, not have a normal pH (C) or alkalemic pH (D)