 Acidosis
Quote:
Acidosis, Lactic
Key Features
Essentials of Diagnosis
Severe acidosis with hyperventilation
Blood pH below 7.30
Serum bicarbonate < 15 mEq/L
Anion gap > 15 mEq/L
Absent serum ketones
Serum lactate > 5 mmol/L
General Considerations
Characterized by overproduction of lactic acid (tissue hypoxia), deficient removal (hepatic failure), or both (circulatory collapse)
Occurs often in severely ill patients suffering from
Cardiac decompensation
Respiratory or hepatic failure
Septicemia
Infarction of bowel or extremities
With the discontinuance of phenformin therapy in the United States, lactic acidosis in diabetics is uncommon but occasionally occurs with use of metformin. It must be considered in the acidotic diabetic, especially if the patient is seriously ill
Etiology
Tissue hypoxia, eg, cardiogenic, septic, or hemorrhagic shock; seizure; carbon monoxide or cyanide poisoning
Hepatic failure
Ischemic bowel
Infarction of extremities
Diabetes, especially with metformin use
Ketoacidosis
Renal failure
Infection
Leukemia or lymphoma
Drugs: ethanol, methanol, salicylates, isoniazid
AIDS
Idiopathic
Clinical Findings
Symptoms and Signs
Main clinical feature is marked hyperventilation
When lactic acidosis is secondary to tissue hypoxia or vascular collapse, the clinical presentation is variable, being that of the prevailing catastrophic illness
In idiopathic, or spontaneous, lactic acidosis
Onset is rapid (usually over a few hours)
Blood pressure is normal
Peripheral circulation is good
No cyanosis
Differential Diagnosis
Other causes of metabolic acidosis
Diabetic ketoacidosis
Starvation ketoacidosis
Alcoholic ketoacidosis
Renal failure (acute or chronic)
Ethylene glycol toxicity
Methanol toxicity
Salicylate toxicity
Other: paraldehyde, metformin, isoniazid, iron, rhabdomyolysis
Diagnosis
Laboratory Tests
High anion gap (serum sodium minus the sum of chloride and bicarbonate anions [in mEq/L] should be no greater than 15). A higher value indicates the existence of an abnormal compartment of anions
Plasma bicarbonate and blood pH are quite low, indicating the presence of severe metabolic acidosis
Ketones are usually absent from plasma and urine, or at least not prominent
In the absence of azotemia, hyperphosphatemia occurs in lactic acidosis for reasons that are not clear
The diagnosis is confirmed by demonstrating, in a sample of blood that is promptly chilled and separated, a plasma lactic acid concentration of 5 mmol/L or higher (values as high as 30 mmol/L have been reported)
Normal plasma values average 1 mmol/L, with a normal lactatepyruvate ratio of 10:1. This ratio is greatly exceeded in lactic acidosis
Treatment
Empiric antibiotic coverage for sepsis should be given after culture samples are obtained if the cause of lactic acidosis is unknown
Alkalinization with IV sodium bicarbonate to keep the pH above 7.2 in the emergency treatment of lactic acidosis is controversial; as much as 2000 mEq in 24 h has been used. However, there is no evidence that the mortality rate is favorably affected by administering bicarbonate
Therapeutic Procedures
Aggressive treatment of the precipitating cause is the main component of therapy, such as ensuring adequate oxygenation and vascular perfusion of tissues
Hemodialysis may be useful when large sodium loads are poorly tolerated
Outcome
Prognosis
Mortality rate of spontaneous lactic acidosis is high
Early and aggressive treatment of metformin-induced lactic acidosis with hemofiltration improves outcome
Prognosis in most cases is that of the primary disorder that produced the lactic acidosis
When to Admit
All patients because of the high mortality rate
Evidence
Practice Guidelines
National Guideline Clearinghouse: Surviving Sepsis Campaign Guidelines for Management of Severe Sepsis and Septic Shock
References
Forsythe SM et al. Sodium bicarbonate for the treatment of lactic acidosis. Chest. 2000 Jan;117(1):2607. [PMID: 10631227]
Salpeter S et al. Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Cochrane Database Syst Rev. 2006 Jan 25;(1):CD002967. [PMID: 16437448]
Content adapted from CURRENT Medical Diagnosis & Treatment 2008 and CURRENT Consult Medicine 2007.
| Quote:
Acidosis, Metabolic, Decreased or Normal Anion Gap
Key Features
Essentials of Diagnosis
The hallmark of this disorder is that the low HCO3 of metabolic acidosis is associated with hyperchloremia, so that the anion gap remains normal
Decreased HCO3 is seen also in respiratory alkalosis, but the pH distinguishes between the two disorders
General Considerations
Most common causes
Gastrointestinal (GI) HCO3 loss
Defects in renal acidification (renal tubular acidoses)
The urinary anion gap can differentiate between these two causes
Renal tubular acidosis (RTA)
Hyperchloremic acidosis with a normal anion gap and normal or near normal glomerular filtration rate, in the absence of diarrhea
Three major types of RTA can be differentiated by the clinical setting: urinary pH, urinary anion gap (see below), serum K+ level
HCO3 loss
Normal anion gap (612 mEq)
GI loss of HCO3, eg, diarrhea, pancreatic ileostomy, or ileal loop bladder
RTA
Recovery from diabetic ketoacidosis
Dilutional acidosis from rapid administration of 0.9% NaCl
Carbonic anhydrase inhibitors
Chloride retention or administration of HCl equivalent or NH4Cl
Decreased anion gap (< 6 mEq)
Plasma cell dyscrasias, eg, multiple myeloma (cationic paraproteins accompanied by chloride and bicarbonate)
Bromide or lithium intoxication
Decreased anion gap without acidosis
Hypoalbuminemia (decreased unmeasured anion)
Severe hyperlipidemia
Renal tubular acidoses
Type I (distal H+ secretion defect)
Due to selective deficiency in H+ secretion in the distal nephron
Low serum K+
Despite acidosis, urinary pH cannot be acidified (urine pH > 5.5)
Associated with autoimmune disease, hypercalcemia
Type II (proximal HCO3 reabsorption defect)
Due to a selective defect in the proximal tubule's ability to adequately reabsorb filtered HCO3
Low serum K+
Urine pH < 5.5
Associated with multiple myeloma and drugs, eg, sulfa, carbonic anhydrase inhibitors (acetazolamide)
Type IV (hyporeninemic hypoaldosteronism)
Only RTA characterized by hyperkalemic, hyperchloremic acidosis
Defect is aldosterone deficiency or antagonism, which impairs distal nephron Na+ reabsorption and K+ and H+ excretion
Urine pH < 5.5
Renal salt wasting is frequently present
Most common in diabetic nephropathy, tubulointerstitial renal diseases, AIDS, and hypertensive nephrosclerosis
Clinical Findings
Symptoms and Signs
Symptoms are mainly those of the underlying disorder
Compensatory hyperventilation may be misinterpreted as a primary respiratory disorder
When acidosis is severe, Kussmaul respirations (deep, regular, sighing respirations) occur and are indicative of intense stimulation of the respiratory center
Diagnosis
Laboratory Tests
See Table 21-15
Blood pH, serum HCO3, and PCO2 are decreased
Anion gap is normal (hyperchloremic) or decreased
Hyperkalemia may be seen
Urinary anion gap from a random urine sample ([Na+ + K+] Cl) reflects the ability of the kidney to excrete NH4Cl as in the following equation:
where 80 is the average value for the difference in the urinary anions and cations other than Na+, K+, NH3+, and Cl
Urinary anion gap is equal to 80 NH3+; this gap aids in the distinction between GI and renal causes of hyperchloremic acidosis:
If the cause of the metabolic acidosis is GI
HCO3 loss (diarrhea), renal acidification ability remains normal
NH4Cl excretion increases in response to the acidosis
Urinary anion gap is negative (eg, 30 mEq/L)
If the cause is distal RTA
The kidney is unable to excrete H+ and thus unable to increase NH4Cl excretion
Therefore, urinary anion gap is positive (eg, +25 mEq/L)
In type II (proximal) RTA
The kidney has defective HCO3 reabsorption, leading to increased HCO3 excretion rather than decreased NH4Cl excretion
Thus, the urinary anion gap is often negative
Urinary pH may not as readily differentiate between renal and GI etiologies
Table 21-15. Hyperchloremic, normal anion gap metabolic acidoses.
See also DDx: Metabolic acidosis, normal anion gap
Treatment
Medications
See Table 21-15
Treatment of RTA is mainly achieved by administration of alkali (either as bicarbonate or citrate) to correct metabolic abnormalities and prevent nephrocalcinosis and renal failure
Type I distal RTA
Supplementation of bicarbonate is necessary since acid accumulates systemically
Type II proximal RTA
Correction of low serum bicarbonate is not indicated except in severe cases
Large amounts of alkali (1015 mEq/kg/day) may be required because much of the alkali is secreted into the urine, which exacerbates hypokalemia
A mixture of sodium and potassium salts, such as K-Shohl, is preferred
Outcome
Complications
The hyperkalemia can be exacerbated by drugs, including
Angiotensin-converting enzyme inhibitors
Aldosterone receptor blockers, such as spironolactone
Nonsteroidal anti-inflammatory drugs
When to Refer
If expertise is needed in determining the etiology of the metabolic acidosis
If consultation is needed on whether bicarbonate should be administered
When to Admit
Respiratory muscle weakness from severe hypokalemia
Evidence
Web Site
National Kidney Foundation
Information for Patients
MedlinePlus: Metabolic Acidosis
MedlinePlus: Distal Renal Tubular Acidosis
MedlinePlus: Proximal Renal Tubular Acidosis
National Kidney and Urologic Diseases Information Clearinghouse: Renal Tubular Acidosis
References
Casaletto JJ. Differential diagnosis of metabolic acidosis. Emerg Med Clin North Am. 2005;23:771. [PMID: 15982545]
Eledrisi MS et al. Overview of the diagnosis and management of diabetic ketoacidosis. Am J Med Sci. 2006 May;331(5):24351. [PMID: 16702793]
Forni LG et al. Circulating anions usually associated with the Krebs cycle in patients with metabolic acidosis. Crit Care. 2005 Oct 5;9(5):R5915. [PMID: 16277723]
Matin MJ et al. Use of serum bicarbonate measurement in place of arterial base deficit in the surgical intensive care unit. Arch Surg. 2005 Aug;140(8):74551. [PMID: 16103283]
Moe OW et al. Clinical acid-base pathophysiology: disorders of plasma anion gap. Best Pract Res Clin Endocrinol Metab. 2003 Dec;17(4):55974. [PMID: 14687589]
Rosival V. Metabolic acidosis. Crit Care Med. 2004 Dec;32(12):25634. [PMID: 15599180]
Content adapted from CURRENT Medical Diagnosis & Treatment 2008 and CURRENT Consult Medicine 2007.
| Quote:
Acidosis, Metabolic, Increased Anion Gap
Key Features
Essentials of Diagnosis
Hallmark of this disorder is that metabolic acidosis (thus low HCO3) is associated with normal serum Cl, so that the anion gap increases
Decreased HCO3 is also seen also in respiratory alkalosis, but pH distinguishes between the two disorders
General Considerations
Calculation of the anion gap is useful in determining the cause of the metabolic acidosis
Normochloremic (increased anion gap) metabolic acidosis
Generally results from addition to the blood of nonchloride acids such as lactate, acetoacetate, -hydroxybutyrate, and exogenous toxins (exception: uremia, with underexcretion of organic acids and anions)
Etiology
Lactic acidosis
Type A (tissue hypoxia): cardiogenic, septic, or hemorrhagic shock; seizure; carbon monoxide or cyanide poisoning
Type B (nonhypoxic): hepatic or renal failure, ischemic bowel, diabetes mellitus (especially with metformin use), ketoacidosis, infection, leukemia or lymphoma, drugs (ethanol, methanol, salicylates, isoniazid), AIDS, idiopathic (usually in debilitated patients)
Diabetic ketoacidosis
Starvation ketoacidosis
Alcoholic ketoacidosis
Acid-base disorders in alcoholism are frequently mixed (10% have triple acid-base disorder)
Three types of metabolic acidoses: ketoacidosis, lactic acidosis, and hyperchloremic acidosis from bicarbonate loss in urine from ketonuria
Metabolic alkalosis from volume contraction and vomiting
Respiratory alkalosis from alcohol withdrawal, pain, sepsis, or liver disease
Uremic acidosis (usually at glomerular filtration rate < 20 mL/min)
Ethylene glycol toxicity
Methanol toxicity
Salicylate toxicity (mixed metabolic acidosis with respiratory alkalosis)
Other: paraldehyde, isoniazid, iron, rhabdomyolysis
Clinical Findings
Symptoms and Signs
Symptoms are mainly those of the underlying disorder
Compensatory hyperventilation may be misinterpreted as a primary respiratory disorder
When severe, Kussmaul respirations (deep, regular, sighing respirations indicating intense stimulation of the respiratory center) occur
Diagnosis
Laboratory Tests
See Table 21-13
Blood pH, serum HCO3, and PCO2 are decreased
Anion gap is increased (normochloremic)
Hyperkalemia may be seen
In lactic acidosis, lactate levels are at least 45 mEq/L but commonly 1030 mEq/L
The diagnosis of alcoholic ketoacidosis is supported by the absence of a diabetic history and no evidence of glucose intolerance after initial therapy
Table 21-13. Primary acid-base disorders and expected compensation.
Treatment
Medications
Supplemental HCO3 is indicated for treatment of hyperkalemia but is controversial for treatment of increased anion gap metabolic acidosis
Administration of large amounts of HCO3 may have deleterious effects, including
Hypernatremia
Hyperosmolality
Worsening of intracellular acidosis
In salicylate intoxication, alkali therapy must be started unless blood pH is already alkalinized by respiratory alkalosis, because the increment in pH converts salicylate to more impermeable salicylic acid and thus prevents CNS damage
The amount of HCO3 deficit can be calculated as follows:
Half of the calculated deficit should be administered within the first 34 h to avoid overcorrection and volume overload
In methanol intoxication, ethanol is administered as a competitive substrate for alcohol dehydrogenase, the enzyme that metabolizes methanol to formaldehyde
Therapeutic Procedures
Treatment is aimed at the underlying disorder, such as insulin and volume resuscitation to restore tissue perfusion
Lactate will later be metabolized to produce HCO3 and increase pH
Outcome
Prognosis
The mortality rate of lactic acidosis exceeds 50%
When to Admit
Because of the high mortality rate, all patients with lactic acidosis should be admitted
Most other patients with significant metabolic acidosis are admitted as well
Prevention
Avoid metformin use if there is tissue hypoxia or renal insufficiency
Acute renal failure can occur rarely with the use of radiocontrast agents in patients receiving metformin therapy
Metformin should be temporarily halted on the day of the test and for 2 days after injection of radiocontrast agents to avoid potential lactic acidosis if renal failure occurs
Evidence
Practice Guidelines
American Diabetes Association: Hyperglycemic Crises in Diabetes, 2004
Information for Patients
MedlinePlus: Metabolic Acidosis
American Diabetes Association: Ketoacidosis
MedlinePlus: Alcoholic Ketoacidosis
References
Casaletto JJ. Differential diagnosis of metabolic acidosis. Emerg Med Clin North Am. 2005;23:771. [PMID: 15982545]
Eledrisi MS et al. Overview of the diagnosis and management of diabetic ketoacidosis. Am J Med Sci. 2006 May;331(5):24351. [PMID: 16702793]
Forni LG et al. Circulating anions usually associated with the Krebs cycle in patients with metabolic acidosis. Crit Care. 2005 Oct 5;9(5):R5915. [PMID: 16277723]
Matin MJ et al. Use of serum bicarbonate measurement in place of arterial base deficit in the surgical intensive care unit. Arch Surg. 2005 Aug;140(8):74551. [PMID: 16103283]
Moe OW et al. Clinical acid-base pathophysiology: disorders of plasma anion gap. Best Pract Res Clin Endocrinol Metab. 2003 Dec;17(4):55974. [PMID: 14687589]
Rosival V. Metabolic acidosis. Crit Care Med. 2004 Dec;32(12):25634. [PMID: 15599180]
Content adapted from CURRENT Medical Diagnosis & Treatment 2008 and CURRENT Consult Medicine 2007.
| Quote:
Acidosis, Respiratory
Key Features
Respiratory acidosis results from decreased alveolar ventilation and subsequent hypercapnia
Be mindful of readily reversible causes, such as respiratory depression from opioids
Acid-base compensation
Acute respiratory acidosis: an increase in serum HCO3 of 1 mEq/L per 10 mm Hg increase in PCO2
Chronic respiratory acidosis (after 612 h): an increase in serum HCO3 of 3.5 mEq/L per 10 mm Hg increase in PCO2
When chronic respiratory acidosis is corrected suddenly, there is a 2- to 3-day lag in renal bicarbonate excretion, resulting in posthypercapnic metabolic alkalosis
Clinical Findings
Acute respiratory acidosis: somnolence, confusion, myoclonus, asterixis
Increased intracranial pressure (papilledema, pseudotumor cerebri)
Coma from CO2 narcosis
Diagnosis
Low arterial pH, increased PCO2
Chronic respiratory acidosis: HCO3 may be elevated along with hypochloremia from NH4+ and Cl renal loss (Table 21-13 )
Treatment
Administer naloxone, 0.042.0 mg IV or SQ (or IM) q 2-3 min x 3 doses if needed, for possible opioid overdose
For all forms of respiratory acidosis, treatment must aim to improve ventilation
Content adapted from CURRENT Medical Diagnosis & Treatment 2008 and CURRENT Consult Medicine 2007.
| enjoy and stuudy hard
abhs   |
08-18-2009, 03:42 AM
LinkBacks (?)
Linear Mode
