Thursday, April 29, 2021

Fluid/Electrolyte Abnormalities Case File

Posted By: Medical Group - 4/29/2021 Post Author : Medical Group Post Date : Thursday, April 29, 2021 Post Time : 4/29/2021
Fluid/Electrolyte Abnormalities Case File
Eugene C. Toy, MD, Manuel Suarez, MD, FACCP, Terrence H. Liu, MD, MPH

Case 26
A 66-year-old man was hospitalized two days ago following an acute hemorrhagic stroke. His CT findings demonstrated a left intracerebral hemorrhage with subarachnoid hemorrhage. The patient's Glascow coma score (GCS) is 13. He was admitted to the ICU for monitoring and management of his hypertension. Today, on hospital day 2, you receive a call from the ICU nurse because the patient appears to be more somnolent. The examination reveals that the patient has the same right extremity weakness as before, no new focal  neurological findings. He is lethargic, answers slowly to commands, and appears confused. Are peat brain CT demonstrates no changes from his initial CT. Laboratory  findings reveal WBC 8000 cells/mm3,  hemoglobin/hematocrit 13.4 g/dL and 42%, sodium 124 mmol/L, serum osmolality 288 mOsm/kg (normal: 278-305 mOsm/kg).

 What is the most likely cause of the patient's mental status changes?
 What is the best treatment for this patient?


Fluid/Electrolyte Abnormalities

Summary: A 66-year-old man with intracerebral and subarachnoid hemorrhage develops hyponatremia and mental status changes 2 days after admission to the ICU. 
  • Cause of mental status change: Acute hyponatremia, most likely due to cerebral salt wasting. 
  • Treatment: Correct hyponatremia with normal saline infusion. Recheck serum electrolytes every 2 to 4 hours, and carefully monitor mental status and neurological examination.

  1. To learn to identify the patients "at-risk" for the development of fluid/electrolyte abnormalities.
  2. To learn the detrimental effects of fluid and electrolyte abnormalities and replacement strategies.
This patient was admitted to the ICU for management of hemorrhagic stroke and subarachnoid hemorrhage. Acute changes in mental status necessitate immediate repeat CT of the brain to rule out cerebral vasospasm as the etiology. In this case, the repeat head CT returned with no interval changes. However, laboratory testing reveals an electrolyte abnormality, namely hyponatremia, which may explain the newly altered mental status. Hyponatremia is a common problem in patients with CNS disease because the brain's ability to regulate sodium and water homeostasis is often altered. It is the most common electrolyte abnormality after an aneurysmal subarachnoid hemorrhage (SAH), occurring in 34% of patients after SAH. It usually occurs between the 2nd and 10th post-bleed day, closely paralleling the period of cerebral vasospasm. It is likely due to cerebral salt wasting, but the trigger is unknown. Natriuresis and volume depletion from cerebral salt wasting may contribute to severe vasospasm in SAH. The diagnosis and management of other fluid and electrolyte abnormalities is paramount.

Approach To:
Fluid/Electrolyte Abnormalities

HYPONATREMIA: Serum sodium concentration <135 mmol/L. Hyponatremia is usually asymptomatic unless the absolute level is <120 mmol/L or the change in sodium concentration is very rapid (within hours ).

TOTAL BODY WATER (TBW): The amount of water in the body, estimated as 60% of a person's weight for men, or 50% of a person's weight for women. One-third of the total body water is located in the extracellular fluid (ECF) compartment, whereas two-thirds of the total body water is located in the intracellular fluid (ICF) compartment.

OSMOLALITY: The concentration of solute particles in a solution is referred to as osmotic activity, expressed in osmoles (Osm). Osmolality is the osmotic activity per volume of water and is expressed in mOsm/kg H2O.

PLASMA OSMOLALITY: The primary extracellular solutes are sodium and its anions, chloride and bicarbonate, glucose, and urea. Plasma osmolality can be calculated with the following formula:

Serum osmolality = [Na] X 2 + [glucose]/18 + BUN/2.8.

TONICITY: A measure of the relative osmotic activity in 2 solutions separated by a membrane that is permeable to water but not solutes. Tonicity is also referred to as effective osmolality.

PLASMA TONICITY: The cell membrane is permeable to water, but solutes that are unable to move across the cell membrane passively are called "effective" solutes because they create osmotic gradients across cell membranes. These osmotic gradients affect water movement between the ICF and ECF compartments. Because water moves freely between the ICF and ECF, osmolality will always be equivalent in both of these compartments. The effective solutes in the ECF include sodium and its anions, as well as glucose. Urea is able to move freely through the cell membrane. However, it makes up a very small portion of the plasma osmolality. As such, the plasma osmolality can often be considered equivalent to the plasma tonicity, also known as the effective plasma osmolality.

Patients "at-risk" for the development fluid/electrolyte abnormalities include those with pulmonary or mediastinal disease and CNS diseases. Hyponatremia, which manifests as vague constitutional or mental status changes, can be found in up to 15 % to 30% of hospitalized patients. Hyponatremia has the potential to cause substantial morbidity and mortality, and has been identified as an independent risk factor for mortality in hospitalized patients. Moreover, overly rapid correction of chronic hyponatremia can cause severe neurological deficits and death.

Sodium homeostasis: Abnormalities of plasma sodium concentration usually reflect an abnormality in total body water rather than a problem with sodium balance. Total body water and its composition are tightly regulated by both osmotic and nonosmotic processes. Under normal circumstances, plasma osmolality is the major determinant of water balance, where plasma osmolality is maintained at approximately 280 to 295 mOsm/kg by arginine vasopressin (AVP), otherwise known as antidiuretic hormone (ADH). Changes in plasma osmolality are monitored by the host by changes in the size of specialized neurons in the hypothalamus, called osmoreceptors. These changes in tonicity are relayed to the magnocellular neurons in the supraoptic and paraventricular nuclei of the hypothalamus, which synthesize AVP for subsequent storage and release. A n increase i n plasma osmolality triggers the release of AVP, which act on V2 receptors in the kidneys to increase water permeability in the distal tubule and collecting duct of the nephrons, resulting in water retention and a subsequent fall in the osmolality. At serum osmolarity levels >295 mOsm/kg, a person's thirst mechanism is also stimulated, triggering an increase in free-water consumption if the person is able to drink. On the contrary, a decrease in plasma osmolality of just 1% to 2% with water intake suppresses AVP secretion and leads to urinary excretion of excess water, thus raising the plasma osmolality back toward normal.

Plasma AVP is also regulated by nonosmotic factors, such as blood pressure and circulating blood volume. Arterial stretch baroreceptors are located in the carotid sinus, aortic arch, cardiac atria, and pulmonary venous system. With an 8% to 10% decrease in arterial pressure, the baroreceptors signal the hypothalamus to release AVP into the plasma. The circulating AVP acts on V2 receptors in the kidney,
increasing free-water reabsorption. In addition, AVP acts on V1 receptors on blood vessels, causing an increase in vascular resistance and in blood pressure. When hyponatremia is with associated hypovolemia, the nonosmotic stimulation of AVP can cause an increase in water retention and worsening of hyponatremia, despite the presence of hypo-osmolality. During periods of low blood volume or blood pressure, baroreceptors in the cardiac atria stimulate the adrenal release of aldosterone, which contributes to sodium and water reabsorption via the proximal renal tubule.

Hyponatremia usually is a result of dysregulation of the tightly regulated process described earlier. As such, persons at risk of developing hyponatremia include those patients who are likely to have disrupted control over their water homeostasis. Risk factors for the development of hyponatremia include head or other traumatic injury, subarachnoid hemorrhage (SAH), acute meningitis, transsphenoidal surgery, other general surgical operations, medications (ie, carbamazepine) , and advancing age (due to a decline in blood flow to the kidney and GFR with age).

Detrimental effects of fluid and electrolyte abnormalities and replacement strategies: The detrimental effects of fluid and electrolyte imbalance in the intensive care unit can evolve as the result of pathologic states or iatrogenically.

Symptomatic hyponatremia usually occurs with absolute sodium levels <120 mmol/L. However, symptoms may also arise secondary to very rapid changes in the serum sodium concentration. Acute hyponatremia is classified as occurring within 48 hours, whereas chronic hyponatremia takes >48 hours to develop. Initial symptoms associated with hyponatremia can be mild, including headache, nausea and vomiting, muscle cramps, aches, or generalized restlessness. With increasing severity, patients may become apathetic, lethargic, or acutely confused. If left undiagnosed and untreated, hyponatremia can progress to seizures, apnea, coma, and death. These symptoms are the manifestations of cerebral edema progression.

Hyponatremia in most cases reflects a state of relative intravascular and extravascular free-water excess, which causes water in the extracellular space to move across the cell membrane into the intracellular space, leading to cell swelling. Within the calvarium, because the skull provides a finite space for the brain to expand, cerebral edema that is left uncorrected can lead to the symptoms detailed earlier as well as eventual brain herniation and death.

Adaptive processes to cerebral edema in the brain include shifting of intracellular potassium to the extracellular fluid, thereby decreasing intracellular osmolality. As a result, brain cells lose water, and globally, the brain returns to normal volume within the skull. This occurs within hours of the onset of cerebral edema. The brain's acute adaptation helps explain why hyponatremia often remains asymptomatic except with rapid changes in sodium concentrations.

Though the brain has developed adaptive processes to deal with imbalances in body water and solute homeostasis, these adaptive processes occur at the expense of losing intracellular potassium and organic osmolytes in the brain. This becomes relevant during the treatment of hyponatremia, particularly chronic hyponatremia. Treatment for hypotonic hyponatremia causes a rise in the serum osmolality toward normal ranges, which draws water out of brain cells as the total body water equilibrates. When the movement of water out of the neurons occurs too rapidly, brain cells that have previously adapted may not have enough time to re-accumulate the intracellular potassium and organic osmolytes that were lost. Consequently, neurons may shrivel and become prone to risk for osmotic demyelination. For unknown reasons, the areas of the brain that are most sensitive to this process are near the pons. Patients who are at high risk of osmotic demyelination after acutely correcting chronic hyponatremia include those with severe malnutrition, alcoholism, or advanced liver disease.

Osmotic demyelination often presents after a period of initial improvement from the symptoms of severe hyponatremia. Several days after correction, new and progressive neurologic symptoms may develop, including spastic quadriparesis or quadriplegia, pseudobulbar palsy, and changes in levels of consciousness. This diagnosis can be established by brain MRI to assess for demyelinated regions in the brain.

Diagnosis and Management
Management of hyponatremia begins with a precise, often multistep, diagnostic algorithm that helps pinpoint the cause of hyponatremia to guide its treatment. This diagnostic process is multistep because hyponatremia can be categorized according to different etiologies that culminate in one similar clinical presentation. For example, unlike hypernatremia, which always is associated with hypertonicity, hyponatremia can occur in the settings of hypotonicity, isotonicity, or hypertonicity. Thus, the first step in patient evaluation is to measure the serum osmolality. Hypertonic hyponatremia occurs when effective solutes other than sodium, such as glucose or mannitol, accumulate in the ECF compartment. These solutes draw water from within cells into the extracellular space, resulting in a hypertonic hyponatremia as the sodium concentration is diluted. A rise in the serum glucose of 100 mg/dL will cause a fall of ∽ 1.6 mmol/L in serum sodium concentration. Isotonic hyponatremia, also called pseudohyponatremia, is usually produced by lab artifacts caused by severe hypertriglyceridemia, hypercholesterolemia, or paraproteinemia that causes measured serum sodium levels to be falsely low while serum osmolality remains normal. Isotonic hyponatremia should trigger a search for an underlying cause of increased serum lipids or paraproteins. Treatment for hypertonic and isotonic hyponatremia centers on treating the underlying cause.

Hypotonic hyponatremia can be dilutional or depletional. Dilutional hyponatremia occurs when extracellular sodium concentrations are low relative to increases in total body water, and this can take place under 2 different scenarios: 1) The absolute sodium level may stay the same, but the total body water increases; and 2) the absolute sodium level increases, but not as much as the total body water, leading to a relative dilution of sodium concentration. Depletional hyponatremia develops when sodium loss outpaces water loss.

After establishing a patient's low serum osmolality, the diagnosis of hypotonic hyponatremia requires further investigation. The next step in diagnosis is to assess the patient's volume status. This is done using a combination of clinical and laboratory signs. Examination of the patient should include assessment of weight changes, orthostatic variations in vital signs, skin turgor (less useful in elderly patients), jugular venous pressure, central venous pressure if central access is available, and an echocardiogram to assess cardiac filling and inferior vena cava engorgement or compressibility. Laboratory measures of fluid status include hemo-concentration or - dilution and the BUN/Cr ratio. Evaluating volume status allows for the placement of a patient's hypotonic hyponatremia into 3 categories: hypovolemia, euvolemia, and hypervolemia.

Hypovolemic hyponatremia is depletional, and can be caused by either renal or extrarenal loss of sodium. Causes of renal sodium loss include diuretic use, cerebral salt wasting syndrome, mineralocorticoid deficiency, and salt-wasting nephropathy. Causes of extrarenal loss of sodium include gastrointestinal losses via vomiting or diarrhea, third space losses from bowel obstruction, pancreatitis, or burns, or sweat losses from endurance exercises. Differentiating between renal and extrarenal sodium loss is done by measuring urine sodium excretion. If the kidney is the site of sodium loss, a spot urine sodium concentration will be >20 mmol/L. On the contrary, a urine sodium concentration of <20 mmol/L points to an extrarenal etiology of sodium loss.

Euvolemic hyponatremia has many causes, the most common being SIADH. 
The diagnosis of SIADH remains a diagnosis of exclusion and requires a demonstration of (1) hyponatremia, (2) low serum osmolality, (3) inappropriately concentrated urine (UOSM> 100 mOsm/kg), (4) persistent urinary sodium excretion (UNa >20 mmol/L) , and (5) exclusion of hypothyroidism or hypoadrenalism. There must also be an absence of any stimuli that might explain an increased secretion of AVP, such as hypovolemia and hypotension. If a measure of the urine osmolality returns with appropriately dilute urine (UOSM <100 mOsm/kg), the cause of hyponatremia can be explained by excessive water intake (primary polydipsia or beer potomania ).

Hypervolemic hyponatremia is caused by clinical entities of volume overload, such as congestive heart failure (CHF), cirrhosis, nephrotic syndrome, and other renal failure.

Distinguishing between SIADH and cerebral salt wasting is important in the management of patients with CNS injury. The biggest distinction between the two pathological entities is that SIADH is a volume-expanded state, whereas cerebral salt wasting is a volume-depleted state. In SIADH, despite low serum osmolality, increased expression of AVP leads to an ongoing dilutional hyponatremia. However, patients are not clinically hypervolemic because only one-third of the total retained water remains in the extracellular space. Cerebral salt wasting, on the contrary, is a state characterized by hypovolemia secondary to primary natriuresis. As such, patients have a negative sodium balance. Though the pathogenesis of cerebral salt wasting is not definitive, it is theorized that impaired sodium reabsorption occurs in the proximal nephron. Reduced sympathetic tone may explain the failure of renin and aldosterone levels to rise despite volume depletion. Volume depletion will ultimately trigger AVP release despite the low serum osmolality, often causing confusion between a diagnosis of SIADH and CSW. However, CSW is always associated with an initial presentation of volume contraction and negative sodium balance.

The goals of treating hyponatremia are (1) to achieve euvolemia and (2) to correct low sodium levels to a safe, but not necessarily normal, range in a controlled manner to avoid the potential of osmotic demyelination. In the case of hypovolemic hypotonic hyponatremia, including cerebral salt wasting seen in SAH, volume replacement with normal saline (0.9% NaCl in water) to euvolemia generally is enough to correct the low sodium level. With volume expansion, the trigger for nonosmotic AVP release is taken away, and the kidneys will then excrete excess free water and correct the serum sodium concentration toward normal. For symptomatic hyponatremia in euvolemic or hypervolemic contexts, correction of sodium levels should take place with hypertonic saline (3% NaCl in water). Because of the risk of osmotic demyelination, this should happen in a controlled manner. Osmotic demyelination can be avoided by limiting correction of hyponatremia to <10 to 12 mmol/L in 24 hours and to <18 mmol/L in 48 hours. Rate of correction should be even slower in patients with risk factors such as severe malnutrition, alcoholism, or advanced liver disease. Acute treatment should be stopped once the patient's symptoms resolve, a safe serum sodium level ( >120 mmol/L) is achieved, or a total magnitude of correction of 18 mmol/L is achieved. During this acute treatment phase, serum sodium levels should be monitored at frequent intervals (every 2-4 hours) .

How does one estimate the amount of infusion of hypertonic saline needed to stay within the safe rates of correction? Adrogue and Madias in 2000 published a seminal article on hyponatremia that included a formula that can be used to calculate the effect of 1 L of infusate on the serum sodium.

Change in serum Na+ = (Infusate Na+ - serum Na+)/(TBW + 1)

Along with acute reversal of symptomatic hyponatremia, fluid restriction is warranted for euvolemic and hypervolemic hyponatremia. All fluids, not only water, need to be restricted. Nonfood fluids should be limited to 500 mL/d below the average daily urine volume. Several days of restriction are needed to make a significant change in the plasma osmolality. Alternative therapy in cases of SIADH includes demeclocycline, which induces a nephrogenic form of diabetes insipidus and excretion of excess free water.

Research is currently underway for new treatments for hyponatremia. The FDA has approved conivaptan, a nonselective vasopressin receptor antagonist, for 4-day IV use to treat euvolemic and hypervolemic hyponatremia. However, the use of this medication in patients with advanced cirrhosis is cautioned, as it also antagonizes

V1 receptors in the splanchnic region, thus increasing splanchnic flow and further elevating portal pressures in patients with liver disease; this predisposes to esophageal bleeding. Because of these concerns, selective V2 receptor antagonists are currently being tested in phase 3 clinical studies.

Beyond disturbances in body water and sodium homeostasis, other electrolyte abnormalities in critically ill patients are also common and associated with poor patient outcomes. The following is a discussion on 3 electrolytes that are commonly measured daily in the intensive care unit: potassium, magnesium, and phosphorus. For a summary of causes of abnormalities in these 3 electrolytes, please refer to Table 26- 1.

Potassium is the body's predominant intracellular cation. The importance of potassium lies in the fact that potassium is the primary determinant of a cell's resting membrane potential. However, only 2% of the body's total potassium stores are found in the ECF, making plasma potassium concentration an insensitive marker of changes in the total body potassium level. Furthermore, the plasma potassium concentration is regulated by a variety of signals, including catecholamines, the reninangiotensis- aldosterone system, glucose and insulin metabolism, and direct release from exercising or injured muscle. Nevertheless, because potassium is essential for cellular functions, it is important to maintain the potassium level in the normal range (3.5 to 5 mEq/L).

Hypokalemia: [K] <3.5 mEq/L can be caused by transcellular shifts or total body potassium depletion. Transcellular shifts occur when potassium moves between the ICF and the ECF Despite the low measured serum potassium, these states do not represent true depletion. Factors that shift potassium into cells include β-agonists (such as albuterol), insulin, alkalosis, and hypothermia. Hypokalemia due to potassium depletion, on the other hand, represents a decrease in total body potassium stores and can be caused by either renal or extra-renal etiologies. For example, diuretics increase sodium delivery to the renal collecting ducts by blocking more proximal tubular sodium reabsorption; this produces a rise in electrochemical gradient in the collecting ducts favoring sodium reabsorption at the expense of potassium secretion. Hypokalemia can occur from extra-renal sources such as from gastrointestinal losses. In patient with excess GI secretion losses, the chloride loss activates the renin-angiotensin-aldosterone system, resulting in renal potassium wasting.

Hypokalemia is generally asymptomatic; however, severe hypokalemia can present as diffuse muscle weakness, EKG changes (U waves, flat or inverted T waves, prolonged QT interval) , ileus, and constipation. Although hypokalemia usually does not produce serious arrhythmias, this condition can potentiate arrhythmias. The first goal of potassium replacement is to eliminate or treat the condition underlying a transcellular shift. The second goal is to replace the serum potassium to a concentration of 4 mEq/L, which can be accomplished with an IV or PO dose of potassium chloride. It should be noted that magnesium depletion impairs potassium reabsorption across the renal tubules, and hypomagnesemia (see the next section)

electrolyte abnornalities in the icu

can be a cause of refractory hypokalemia. A s such, magnesium also must be replaced to a normal level when replacing serum potassium.

Hyperkalemia: [K] >5.5 mEq/L is often more clinically apparent in comparison to hypokalemia. It is associated with slowing of cardiac electrical conduction and manifests with classic ECG findings. These include peaked T waves, decreased amplitude of the P wave, increased PR interval, loss of P waves, and eventually QRS prolongation that can lead to asystole if left untreated. However, hyperkalemia can often be spurious due to traumatic venipuncture and subsequent potassium release, or specimen hemolysis. Thus, unexpected hyperkalemia should be validated with repeat blood draw if possible.

The causes of hyperkalemia can also be categorized as transcellular shifts versus impaired renal excretion. Impaired renal excretion in critical care patients is mostly due to renal insufficiency. Adrenal insufficiency can also be a cause of hyperkalemia, but this is not commonly seen in ICU patients. Furthermore, many drugs, such as sulfamethoxazole (Bactrim), subcutaneous heparin, and pentamidine can cause hyperkalemia by inhibiting the renin-angiotensin-aldosterone system. Lastly, blood transfusions can contribute to hyperkalemia, as the potassium in stored erythrocytes leaks out slowly. The accumulation of extracellular potassium in stored blood is usually cleared renally in patients receiving transfusions, but this may become a problem in patients with acute renal failure or hemodynamic shock.

There are 3 ways of managing hyperkalemia. First, to inhibit the arrhythmogenic nature of hyperkalemia, calcium infusions are used to stabilize the myocardium. These infusions are temporary, lasting 20 to 30 minutes, and will temporize the condition until the effects of definitive measures take place. Second, medications that shift potassium from the ECF to the ICF are employed to temporarily decrease the plasma potassium concentrations. These include insulin and glucose, albuterol, and bicarbonate. Note, however, that bicarbonate actually has little clinical value because it binds to calcium in the plasma, which would render our calcium infusion ineffective if given together. Third, more definitive measures should be undertaken to remove excess potassium from the body. These include sodium polystyrene (Kayexalate), a cation exchange resin, furosemide, a loop diuretic that enhances urinary potassium excretion, and dialysis, the most effective method in patients with acute renal failure.

As the body's second most abundant cation, magnesium serves as an important cofactor in a multitude of enzyme reactions. One such magnesium-dependent system is the membrane pump that generates a cell's resting membrane potential. Magnesium is also responsible for regulating calcium movement into smooth muscle cells. As such, it is essential in helping the body maintain cardiac contractility and peripheral vascular tone. These functions make it important for magnesium levels in the plasma to be maintained at normal values.

Hypomagnesemia, defined as a serum magnesium concentration <2 mEq/L, occurs in 20% of hospitalized patients and 65 % of ICU patients. Diuretics can cause hypomagnesemia, as inhibition of sodium reabsorption interferes with magnesium reabsorption. The gastrointestinal tract can also be a direct source of magnesium depletion.

Diarrhea leads to a loss of magnesium; therefore, short gut syndrome and other malabsorptive states are associated with decreased magnesium absorption. Furthermore, in patients with chronic and heavy alcohol use, hypomagnesemia in the ICU may be exacerbated by depleted total body stores produced by chronic malnutrition, diarrhea, and thiamine deficiency associated with chronic alcohol abuse.

Similar to potassium, deficiencies in plasma magnesium are largely asymptomatic. However, when manifested, symptoms include weakness, tetany, and seizures. Beyond its essential role in many of the body's enzymatic reactions, magnesium replacement is important because hypomagnesemia is usually associated with other electrolyte abnormalities that will be refractory to treatment unless the magnesium level is normal. Magnesium replacement is accomplished with IV infusions of magnesium sulfate in normal saline.

Phosphorus is an important electrolyte because of its participation in aerobic energy production. The presentation of phosphorus abnormalities is usually subclinical, though impaired cellular energy production may develop secondary to hypophosphatemia and can be detrimental to systemic oxygen delivery. Decreased energy production in the heart can cause decreased inotropy and cardiac output. Hypophosphatemia is also associated with reduced deformability of red blood cells, leading to hemolytic anemia. Lastly, low phosphate levels are associated with low levels of 2,3-DPG, which shifts the oxygen-hemoglobin dissociation curve to the left and reduces the release of oxygen to tissues.

Hypophosphatemia is defined as a plasma phosphate concentration of < 2.5 mg/dL and can be caused by many factors. Glucose loads can decrease ECF phosphate as phosphate enters cells along with glucose. The use of phosphate binders, such as sucralfate, can iatrogenically lower the phosphate level in the serum. The reintroduction of nutrition in patients with prolonged periods of nonfeeding can cause low phosphate levels via the refeeding syndrome. Hypophosphatemia is also commonly seen in patients with respiratory alkalosis, sepsis, and DKA. Phosphate replacement is accomplished with IV or PO preparations of potassium phosphate or sodium phosphate.

  • See also case Case 23 (Acute Kidney Injury), Cases 24 and 25 (Acid-Base Abnormalities I and II) , and Case 27 (Traumatic Brain Injury).


26.1  A 53 -year-old woman with a history of uncontrolled hypertension is admitted to the ICU with subarachnoid hemorrhage. She has had endovascular coiling of an anterior communicating artery aneurysm. On post-procedure day 4, she becomes acutely confused and lethargic. On evaluation of the patient, you find her vital signs to be the following: temperature 37.5 °C, HR 110 beats/minute, BP 150/90 mm Hg, RR 16 breaths/min, O2 saturation 98% on 2L/min oxygen by nasal cannula. She is somnolent, oriented only to person, and has a GCS of E3 V4 M6 (13). She has no focal neurologic deficits. Her mucous membranes are dry, her urine output has been 25 mL/h in the past 2 hours, and her CVP is 5 . While awaiting a repeat CT scan o f the head, laboratory values return and reveal serum sodium of 128 mmol/L and serum osmolarity of 260 mOsm/kg water. What is your next step in management of this patient?
A. Fluid bolus with 3 % NS.
B. Fluid bolus with 0.9% NS.
C. Fluid restriction.
D. Give demeclocycline.
E. Give the patient salt tabs to take PO.
F. Urgent hemodialysis.

26.2 An otherwise healthy 40-year-old woman with a history of remote appendectomy is postoperative day 5 after an exploratory laparotomy and adhesiolysis for complete bowel obstruction. Yesterday, her nasogastric tube was removed and she was started on a clear liquid diet. You are notified by her nurse to evaluate her for altered mental status . Upon your evaluation, she is confused and agitated. Her vital signs are stable and normal. She is clinically euvolemic and weighs 60 kg. Laboratory testing reveals a serum sodium concentration of 122 mmol/L and serum osmolarity of 240 mOsm/kg water. You decide to correct her hyponatremia using 3% saline. At what rate will you run your infusion for the next 12 to 24 hours?
A. 33 mL/h.
B. 66 mL/h.
C. 1 00 mL/h.
D. Give the infusion as a bolus over 1 hour.
E. 133 mL/h.

26.3  An 1 8-year-old gentleman is intubated and sedated in your ICU following an exploratory laparotomy for multiple gunshot wounds to the abdomen. On postoperative day 1, morning labs reveal a serum potassium concentration of 6.2 mmol/L. Which of the following is the LEAST IMPORTANT part of your initial evaluation and management of this patient?
A. Repeat potassium measurement
B. 12-lead ECG
C. Infusion of calcium gluconate
D. Treatment with insulin and glucose
E. Fluid bolus with 0.9% saline


26.1  B. The patient in question has had coiling of an intracerebral aneurysm. She most likely presents with altered mental status due to hyponatremia secondary to cerebral salt wasting syndrome. Several clues in the vignette help you decide that she is clinically hypovolemic (mild tachycardia, low urine output, dry mucous membranes, and low CVP). The first goal of treating symptomatic hyponatremia is to achieve euvolemia. As such, this woman should be fluid bolused with an isotonic solution, such as normal saline. Once euvolemia is achieved, the impetus for nonosmotic AVP release is resolved. If the patient still remains symptomatic at that time, considerations should then be made for correction with hypertonic saline.

26.2  A. The patient in question weighs 60 kg, and as such, her TBW is estimated at 30 L (0.5 X 60). Using the equation from Adrogue et al, infusion of a liter of 3% saline will change the serum concentration by 12.7 mmol. The calculation is done below:

3% Saline = 513 mmol/L of sodium
Patient's serum sodium = 122 mmol/L
TBW = 30
Change in serum [Na] = (513 - 122)/(30 + 1) = 12.7 mmol

A safe target for correction of serum sodium is 10 mmol in 24 hours. For this patient, a correction of 10 mmol would take 790 mL (10/12.7 = .79). To infuse 790 mL over 24 hours would take a rate of 33 mL/h.

26.3  E. The evaluation and treatment of hyperkalemia involves all of the aforementioned answers except for fluid boluses. Repeat measurements should be pursued to confirm a true hyperkalemia. An ECG should be performed to assess for myocardial instability. A calcium infusion should be given to stabilize the myocardium. Temporary correction of hyperkalemia can be done with albuterol or insulin. More definitive treatment includes giving polystyrene (Kayexalate), furosemide, or undergoing hemodialysis if the patient is in acute renal failure. There is no role for fluid boluses in the management of hyperkalemia.

 High-risk patients for osmotic demyelination after acutely correcting chronic hyponatremia include those with severe  malnutrition, alcohol­ism, or advanced liver disease. 
 Osmotic demyelination associated with hyponatremia treatment can be avoided  by limiting correction of hyponatremia to <10 to 12 mmol/L in 24 hours and to <18 mmol/L in 48 hours. 
 Treatment of hyperkalemia include several categories: temporary - insulin + glucose, sodium bicarbonate; membrane stabilization - calcium infusion; elimination (definitive) - sodium polysty - rene (Kayexelate), loop diuretics, and hemodyalsis.


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