GU/neprho
In this section, we will be talking about the following:
Acid/Base
Electrolytes
AKI
Acid/Base
The management of acid/base disturbances is a fundamental aspect of patient care. These disturbances can arise from various underlying conditions, including sepsis, renal failure, or pulmonary disorders. Healthcare professionals closely monitor patients' arterial blood gases and electrolyte levels, intervening with appropriate treatments like correcting the underlying cause, administering bicarbonate for severe acidosis, or adjusting ventilator settings to address respiratory issues. The body's ability to maintain a delicate balance between acids and bases is crucial for normal physiological functioning.
Importance of pH Regulation
pH is a measure of the acidity or alkalinity of a solution and is determined by the concentration of hydrogen ions (H+) present. In the human body, the pH of various fluids and tissues must be tightly regulated to ensure optimal cellular function. The normal pH range for arterial blood is approximately 7.35 to 7.45, with a slightly alkaline pH being preferred.
Maintaining the appropriate pH is REALLY important because even slight deviations can have significant physiological consequences. Acidosis, which refers to a decrease in pH below the normal range, can lead to impaired cellular function, altered enzyme activity, and disruption of normal physiological processes. Alkalosis, on the other hand, is characterized by an increase in pH above the normal range and can also have detrimental effects on cellular function.
Role of Buffers
Buffers play a vital role in maintaining acid/base balance by minimizing changes in pH. Buffers are substances that can accept or donate hydrogen ions, thereby stabilizing the pH of a solution. The bicarbonate buffer system is the most important buffer system in the human body and operates in both the extracellular and intracellular compartments.
In the bicarbonate buffer system, carbonic acid (H2CO3) acts as a weak acid, and bicarbonate ions (HCO3-) act as a weak base. When there is an excess of hydrogen ions, the bicarbonate ions combine with them to form carbonic acid, which can then be converted to water and carbon dioxide through the action of the enzyme carbonic anhydrase. Conversely, when there is a deficit of hydrogen ions, carbonic acid dissociates, releasing bicarbonate ions and hydrogen ions.
Other buffer systems, such as the phosphate buffer system and the protein buffer system, also contribute to maintaining acid/base balance. These systems work in a similar manner, accepting or donating hydrogen ions as needed to stabilize pH.
Acid/Base Disorders
Acid/base disorders occur when there is an imbalance in the production, elimination, or buffering of acids and bases in the body. These disorders can be broadly classified into two categories: respiratory and metabolic.
Respiratory acid/base disorders result from changes in the levels of carbon dioxide (CO2) in the blood, which in turn affect the concentration of carbonic acid. Respiratory acidosis occurs when there is an increase in CO2 levels, leading to an accumulation of carbonic acid and a decrease in pH. Conversely, respiratory alkalosis occurs when there is a decrease in CO2 levels, resulting in a decrease in carbonic acid and an increase in pH.
Metabolic acid/base disorders, on the other hand, are caused by changes in the levels of bicarbonate ions in the blood. Metabolic acidosis occurs when there is a decrease in bicarbonate levels, leading to an increase in hydrogen ions and a decrease in pH. Metabolic alkalosis occurs when there is an increase in bicarbonate levels, resulting in a decrease in hydrogen ions and an increase in pH.
Compensatory Mechanisms
The body has several compensatory mechanisms to restore acid/base balance in the event of an acid/base disorder. These mechanisms aim to either increase or decrease the levels of carbon dioxide or bicarbonate ions to counteract the primary disturbance.
In respiratory acid/base disorders, the kidneys play a crucial role in compensating for the primary disturbance. The kidneys can adjust the excretion or reabsorption of bicarbonate ions to restore balance. In metabolic acid/base disorders, the respiratory system compensates by altering the rate and depth of breathing to regulate carbon dioxide levels.
It is important to note that compensatory mechanisms may take time to fully restore acid/base balance, and in some cases, they may not be able to completely compensate for the primary disturbance.
Resources to complete:
FCCS Ch. 6 (part of it)
Marino 3rd ed: Ch 28-30; 4th ed 31-33
Acid-Base, Fluid, Electrolytes made ridiculously simple (PRIMARY RESOURCE)
MedCram: Medical Acid Base videos 1-8
Pulmcast: Back to the #Basics (Bicarb)
Fluid and Electrolytes
Electrolytes are essential minerals that play a crucial role in maintaining the normal functioning of the human body. They are electrically charged particles that are found in bodily fluids, including blood, urine, and tissue fluid. These electrolytes include sodium, potassium, calcium, magnesium, phosphorus, and bicarbonate. Each electrolyte has specific functions and plays a vital role in various physiological processes.
Sodium is the most abundant electrolyte in extracellular fluid and plays a crucial role in maintaining fluid balance, nerve function, and muscle contraction. It helps regulate blood pressure and is essential for the transmission of nerve impulses. Sodium levels are tightly regulated by the kidneys and the hormone aldosterone.
Potassium is the primary electrolyte found inside cells and is crucial for maintaining proper cell function, nerve transmission, and muscle contraction. It plays a vital role in regulating heart rhythm and blood pressure. Potassium levels are regulated by the kidneys and the hormone aldosterone.
Calcium is essential for bone health, muscle contraction, nerve function, and blood clotting. It plays a crucial role in maintaining the integrity of the skeletal system and is involved in various enzymatic reactions. Calcium levels are regulated by parathyroid hormone (PTH), calcitonin, and vitamin D. Total calcium levels can be affected by albumin levels, so corrected calcium calculations may be necessary. Ionized calcium is the physiologically active form and provides a more accurate assessment of calcium status.
Magnesium is involved in over 300 enzymatic reactions in the body and plays a vital role in muscle and nerve function, protein synthesis, and energy production. It is also essential for maintaining a normal heart rhythm and blood pressure. Magnesium levels are regulated by the kidneys.
Phosphorus is a key component of DNA, RNA, and ATP (adenosine triphosphate), the energy currency of the body. It is essential for bone health, cell membrane structure, and acid-base balance. Phosphorus levels are regulated by parathyroid hormone (PTH) and vitamin D.
Bicarbonate is an important electrolyte involved in maintaining acid-base balance in the body. It acts as a buffer, helping to regulate the pH of bodily fluids. Bicarbonate levels are regulated by the kidneys and the respiratory system.
These electrolytes work together to maintain the balance of fluids inside and outside cells, regulate nerve and muscle function, and support various biochemical reactions in the body. Imbalances in electrolyte levels can have significant consequences on overall health and can lead to various disorders.
In the ICU, electrolyte disorders are common due to the critical nature of the patients' conditions and the interventions they undergo. These disorders can arise from a variety of causes, including underlying medical conditions, medications, fluid imbalances, and organ dysfunction. It is crucial for healthcare professionals in the ICU to closely monitor electrolyte levels and promptly address any imbalances to prevent complications.
Hyponatremia
Hyponatremia can occur due to various mechanisms, including water excess, sodium loss, or a combination of both. The most common cause of hyponatremia in the ICU is the syndrome of inappropriate antidiuretic hormone secretion (SIADH), which leads to water retention and dilutional hyponatremia. Other causes include diuretic use, adrenal insufficiency, renal dysfunction, heart failure, liver cirrhosis, and certain medications.
The diagnosis of hyponatremia involves a comprehensive evaluation of the patient's clinical history, physical examination, and laboratory investigations. Key steps in the diagnostic process include:
Assessment of volume status: Determining whether the patient is hypovolemic, euvolemic, or hypervolemic is crucial in identifying the underlying cause of hyponatremia. This can be done through a combination of clinical examination, urine output measurement, and laboratory tests.
Measurement of serum osmolality: Serum osmolality helps differentiate between hypertonic, isotonic, and hypotonic hyponatremia. Hypotonic hyponatremia is the most common type encountered in the ICU and is characterized by low serum osmolality.
Urine osmolality and sodium concentration: These tests help determine the kidney's ability to concentrate urine and excrete free water appropriately. In SIADH, urine osmolality is typically high, while urine sodium concentration is usually elevated in conditions such as diuretic use or renal dysfunction.
Additional investigations: Depending on the clinical scenario, further investigations such as thyroid function tests, adrenal function tests, and imaging studies may be required to identify the underlying cause of hyponatremia.
Hyperkalemia
Hyperkalemia is usually secondary to one of three things -
Increased intake of potassium
Very rarely do pure dietary excesses of potassium alone cause high potassium levels unless there is a coexistent renal insufficiency or interuption of the renin angiotensin aldosterone mechanisms (e.g. Losartan)
Can be over-replaced in the ICU setting (went from 2.8 to 5.6, then the patient probably recieved too much replacement in the hospital)
Cellular shifts
First, rule out hemolyzed samples - repeat the draw without using a tourniquet and without the patient closing their fist
Rule out rhabdomyolysis - check a CPK level
Thrombcytosis (usually >1 million platelets)
Leukocytosis (in the setting of acute leukemia)
Defect in renal excretion of potassium
Chronic Kidney disease patients (excretory defect)
NSAIDs can cause hypo-reninemic hypoaldosteronism, especially in diabetic patients
Adrenal insufficiency (e.g. higher blood pressure, metabolic acidosis)
Obstructive Uropathy (usually in type IV renal tubular acidosis; check bicarbonate level); can also check renal ultrasound to rule out hydronephrosis
Check renin, aldosterone
2000 mg potassium restricted diet
Hypercalcemia
The differential diagnosis includes PTH mediated and non-PTH mediated. You must first check a PTH level. If the PTH level is ALSO high, you must think of primary hyperparathyroidism.
If the PTH level is low, it means it was appropriately suppressed, and primary hyperparathyroidism is unlikely. Other etiologies of hypercalcemia (in the setting of a low PTH):
Medication related
Taking Vitamin D supplements when your vitamin D level is normal. This is very common.
Chlorthalidone is a thiazide diuretic and it can cause hypercalcemia.
Humoral hypercalcemia - caused by too much parathyroid hormone-related peptide (PTHrP) from malignant tumors.
To rule this out, you must check a PTH related peptide. You can also check CXR or CT of chest and abdomen pelvis to rule out any mass lesions.
Granulomatosis lesions - can cause hypercalcemia usually mediated through excess 1, 25 hydroxyvitamin D levels. This could be secondary to sarcoidosis or lymphomas.
To rule this out, check a 1, 25 hydroxyvitamin D level
Metastatic lesions to the bone or Multiple Myeloma can cause hypercalcemia
Check serum total protein
SPEP
UPEP (urine immunofixation electrophoresis)
Resources to complete:
FCCS Ch. 12
Marino 3rd ed: Ch 32-35; 4th ed: Ch 35-38
Acid-Base, Fluid, Electrolytes made ridiculously simple (PRIMARY RESOURCE)
MedCram: Hyponatremia
AKI
Acute kidney injury (AKI), also known as acute renal failure, is a sudden and rapid decline in kidney function. It is characterized by a sudden decrease in the ability of the kidneys to filter waste products and excess fluid from the blood. This condition can occur within a few hours or days and is often reversible if detected and managed promptly.
The classification of AKI is based on the severity of the condition and the level of kidney function. There are several different classification systems used to categorize AKI, including -
RIFLE (Risk, Injury, Failure, Loss, End-stage kidney disease) criteria
the AKIN (Acute Kidney Injury Network) criteria
the KDIGO (Kidney Disease: Improving Global Outcomes) criteria
The RIFLE criteria classify AKI into five stages based on the level of kidney function and the presence of other markers of kidney damage, such as urine output. The stages range from "Risk" (stage 1) to "Failure" (stage 3), with additional stages for "Loss" (stage 4) and "End-stage kidney disease" (stage 5). The AKIN criteria are similar to the RIFLE criteria but have some modifications in the definition of AKI and the staging system. The KDIGO criteria further refine the classification of AKI by incorporating both the level of kidney function and the duration of the injury.
AKI can be classified into three main types based on the underlying cause: prerenal, intrinsic renal, and postrenal.
Prerenal AKI occurs when there is a decrease in blood flow to the kidneys, leading to reduced oxygen and nutrient supply. This can be caused by conditions such as dehydration, severe blood loss, or decreased cardiac output.
Intrinsic renal AKI is caused by damage to the kidney tissue itself, often due to conditions such as acute tubular necrosis, glomerulonephritis, or interstitial nephritis.
Postrenal AKI occurs when there is an obstruction in the urinary tract, preventing the normal flow of urine. This can be caused by conditions such as kidney stones, tumors, or an enlarged prostate.
Another way to classify AKI is based on the time course of the injury. AKI can be categorized as acute-onset, subacute, or chronic. Acute-onset AKI refers to a sudden decline in kidney function that occurs within a few hours or days. Subacute AKI refers to a slower decline in kidney function over a period of weeks. Chronic AKI refers to a gradual and progressive decline in kidney function over a period of months or years.
It is important to note that AKI is a dynamic condition, and the classification may change over time as the underlying cause is identified and managed. The severity of AKI can also vary, ranging from mild and transient to severe and life-threatening. Prompt recognition and appropriate management of AKI are crucial to prevent further kidney damage and improve patient outcomes.
Causes of AKI
In the ICU setting, AKI can be kind of complex. Pre-renal factors, such as hypovolemia and decreased cardiac output, can lead to decreased renal perfusion and subsequent ischemia. Intrinsic renal factors, including acute tubular necrosis and acute interstitial nephritis, can result from direct renal injury or the effects of systemic inflammation. Post-renal factors, such as urinary tract obstruction, can impair urine flow and lead to kidney injury.
Therefore, in critically ill patients, the development of AKI is often multifactorial. Sepsis, a common condition in the critical care setting, can lead to systemic inflammation and endothelial dysfunction, which can impair renal blood flow and contribute to the development of AKI. Additionally, the use of nephrotoxic medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and certain antibiotics, can further contribute to renal injury in critically ill patients.
Resources to complete: