Lactic acidosis

Septic shock is the subset of sepsis with hypotension requiring vasopressors to maintain a mean arterial pressure above 65 mm Hg plus a serum lactate above 2 mmol/L despite adequate fluid resuscitation, carrying in-hospital mortality of 40% or higher. Management is a timed sequence: 30 mL/kg crystalloid bolus, blood cultures and broad-spectrum antibiotics within 1 hour, norepinephrine titrated to MAP >=65, and escalation to a second vasopressor and stress-dose hydrocortisone when hypotension persists.

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection, identified by an acute rise in SOFA score of 2 points or more in a patient with known or suspected infection. Survival depends on recognizing the pattern early and completing the hour-1 bundle: lactate, blood cultures before antibiotics, broad-spectrum antibiotics such as cefepime 2 g IV every 8 hours, and 30 mL/kg crystalloid for hypotension or a lactate of 4 mmol/L or higher.

Cardiogenic shock is primary cardiac pump failure that produces sustained hypotension and end-organ hypoperfusion despite adequate filling, most often from a large acute myocardial infarction. Survival depends on emergently reversing the cause, usually by revascularization, while supporting perfusion with vasopressors, inotropes, and, when refractory, mechanical circulatory support.

Acute mesenteric ischemia is an abrupt drop in small-bowel blood flow, most often superior mesenteric artery embolism, presenting as severe abdominal pain out of proportion to an unimpressive early examination. CT angiography confirms the diagnosis, and survival depends on immediate resuscitation, antibiotics, and anticoagulation followed by urgent revascularization or resection before infarction and peritonitis develop.

Acute liver failure is the abrupt onset of hepatic synthetic dysfunction, defined by coagulopathy with an INR of 1.5 or higher plus any grade of hepatic encephalopathy, occurring within 26 weeks of illness onset in a patient without preexisting liver disease. Acetaminophen overdose is the leading cause in the United States, and management centers on N-acetylcysteine when acetaminophen is implicated, intensive supportive care, and early referral to a liver transplant center.

Acute kidney injury is a sudden rise in serum creatinine or fall in urine output from prerenal, intrinsic, or postrenal causes, defined and staged by KDIGO criteria. Management targets the underlying cause, corrects volume and electrolyte derangements, and escalates to renal replacement therapy for refractory hyperkalemia, acidosis, volume overload, or uremia.

Carbon monoxide poisoning follows inhalation of a colorless, odorless combustion product that binds hemoglobin roughly 200 to 300 times more avidly than oxygen, producing tissue hypoxia that pulse oximetry cannot detect. Diagnosis requires co-oximetry on a blood gas to measure carboxyhemoglobin. Treatment is immediate high-flow 100% oxygen, escalated to hyperbaric oxygen for loss of consciousness, neurologic or cardiac ischemia, or pregnancy.

Short bowel syndrome is malabsorption from insufficient functional small intestine, usually after massive resection for Crohn disease, mesenteric ischemia, or tumor. Diagnosis rests on residual bowel length and colon continuity; first-line treatment sequences diet, high-dose loperamide, and antisecretory therapy, escalating to parenteral nutrition and teduglutide.

Renal replacement therapy (RRT), intermittent hemodialysis (IHD), continuous renal replacement therapy (CRRT), prolonged intermittent renal replacement therapy (PIRRT), or peritoneal dialysis (PD), substitutes for lost kidney function when acute kidney injury or end-stage kidney disease causes refractory acidosis, hyperkalemia, volume overload, or uremia. Modality is chosen mainly by hemodynamic stability: CRRT or PIRRT for the unstable patient, IHD for rapid clearance of severe hyperkalemia or a dialyzable toxin.

Metabolic acidosis is a primary fall in serum bicarbonate that is first confirmed with an arterial or venous blood gas, then classified by the serum anion gap into an increased anion gap process (unmeasured organic anion, most often lactate) or a normal anion gap process (bicarbonate loss from the gut or kidney). The urine anion gap and clinical context localize the cause, and management targets the underlying disease, reserving intravenous sodium bicarbonate for severe acidemia (pH less than 7.1-7.2) or specific indications such as chronic kidney disease and renal tubular acidosis.