| Hyperkalemia |
|
Electrocardiography showing precordial leads in hyperkalemia.
|
| Classification and external resources |
| ICD-10 |
E87.5 |
| ICD-9 |
276.7 |
| DiseasesDB |
6242 |
| MedlinePlus |
001179 |
| eMedicine |
emerg/261 |
| Patient UK |
Hyperkalemia |
| MeSH |
D006947 |
Hyperkalemia (hyperkalaemia in British English, hyper- high; kalium, potassium; -emia, "in the blood") refers to the condition in which the concentration of the electrolyte potassium (K+) in the blood is elevated. The symptoms of elevated potassium are nonspecific, and the condition is usually discovered on blood tests performed for another reason. Extreme hyperkalemia is a medical emergency due to the risk of potentially fatal abnormal heart rhythms (arrhythmia).
Temporary treatment can be given to reduce the risk of complications, but removal of the excess potassium by stimulating urine production or through dialysis is usually necessary.
Opposite condition: Hypokalemia refers to the condition in which the concentration of potassium (K+) in the blood is low.
Contents
- 1 Signs and symptoms
- 2 Causes
- 2.1 Ineffective elimination
- 2.2 Excessive release from cells
- 2.3 Excessive intake
- 2.4 Lethal injection
- 2.5 Pseudohyperkalemia
- 3 Pathophysiology
- 4 Diagnosis
- 5 Prevention
- 6 Treatment
- 6.1 Myocardial excitability
- 6.2 Temporary measures
- 6.3 Elimination
- 7 Research
- 8 References
- 9 External links
Signs and symptoms
|
|
This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (January 2014) |
Symptoms are fairly nonspecific and generally include malaise, palpitations and muscle weakness;[1] mild hyperventilation may indicate a compensatory response to metabolic acidosis, which is one of the possible causes of hyperkalemia. Often, however, the problem is detected during screening blood tests for a medical disorder, or after hospitalization for complications such as cardiac arrhythmia or sudden cardiac death.
During the medical-history intake, physicians focus on kidney disease and medication use (see below), as these are the main causes. The combination of abdominal pain, hypoglycemia, and hyperpigmentation, often in the context of other autoimmune disorders, may be signs of Addison's disease,[2] which is a medical emergency.
Causes
|
|
This section does not cite any references or sources. Please help improve this section by adding citations to reliable sources. Unsourced material may be challenged and removed. (January 2014) |
Ineffective elimination
- Renal insufficiency
- Medication that interferes with urinary excretion:
- ACE inhibitors and angiotensin receptor blockers
- Potassium-sparing diuretics (e.g. amiloride and spironolactone)
- NSAIDs such as ibuprofen, naproxen, or celecoxib
- The calcineurin inhibitor immunosuppressants ciclosporin and tacrolimus
- The antibiotic trimethoprim
- The antiparasitic drug pentamidine
- Mineralocorticoid deficiency or resistance, such as:
- Addison's disease
- Aldosterone deficiency
- Some forms of congenital adrenal hyperplasia
- Type IV renal tubular acidosis (resistance of renal tubules to aldosterone)
- Gordon's syndrome (pseudohypoaldosteronism type II) ("familial hypertension with hyperkalemia"), a rare genetic disorder caused by defective modulators of salt transporters, including the thiazide-sensitive Na-Cl cotransporter.
Excessive release from cells
- Rhabdomyolysis, burns, or any cause of rapid tissue necrosis, including tumor lysis syndrome
- Massive blood transfusion or massive hemolysis
- Shifts/transport out of cells caused by acidosis, low insulin levels, beta-blocker therapy, digoxin overdose, or the paralyzing agent succinylcholine
- Box jellyfish venom
- Acute Digoxin toxicity may cause hyperkalaemia[3]
Excessive intake
- Excessive intake with potassium salt-substitute, potassium-containing dietary supplements, or potassium chloride (KCl) infusion. Note that, for a person with normal kidney function and normal elimination (see above), hyperkalemia by potassium intake would be seen only with large infusions of KCl or oral doses of several hundred milliequivalents of KCl.[4][unreliable medical source?]
Lethal injection
In the United States of America, hyperkalemia is induced by lethal injection in capital punishment cases. Potassium chloride is the last of the three drugs administered and actually causes death. Injecting potassium chloride into the heart muscle disrupts the signal that tells the heart to beat. This same amount of potassium chloride would do no harm if taken orally and not injected.
Pseudohyperkalemia
Pseudohyperkalemia is a rise in the amount of potassium that occurs due to excessive leakage of potassium from cells, during or after blood is drawn. It is a laboratory artifact rather than a biological abnormality and can be misleading to caregivers.[5][unreliable medical source?] Pseudohyperkalemia is typically caused by hemolysis during venipuncture (by either excessive vacuum of the blood draw or by a collection needle that is of too fine a gauge); excessive tourniquet time or fist clenching during phlebotomy (which presumably leads to efflux of potassium from the muscle cells into the bloodstream);[6][unreliable medical source?] or by a delay in the processing of the blood specimen. It can also occur in specimens from patients with abnormally high numbers of platelets (>500,000/mm³), leukocytes (> 70 000/mm³), or erythrocytes (hematocrit > 55%). People with "leakier" cell membranes have been found, whose blood must be separated immediately to avoid pseudohyperkalemia.[7][unreliable medical source?]
A familial form of pseudohyperkalemia occurs, which is a dominant red-cell trait characterized by increased serum potassium in whole blood stored at or below room temperature, without additional hematological abnormalities.[8][unreliable medical source?] It appears to be due to mutations in Langereis blood group antigen, which encodes an erythrocyte membrane porphyrin transporter. The gene, known as ABCB6, is located on the long arm of chromosome 2 (2q36).
Pathophysiology
Normal serum potassium levels are generally considered to be between 3.5 and 5.0 mEq/L. Levels above 5.0 mEq/L indicate hyperkalemia, and those below 3.5 mgEq/L indicate hypokalemia. Both hyperkalemia and hypokalemia are potentially life-threatening. For example, recent data evaluating the relationship between mortality and levels of potassium in patients with chronic kidney disease who were not on dialysis, found that lower serum potassium levels (i.e., <4.0 mmol/L) were associated with a higher risk of mortality and end-stage renal disease, compared with serum potassium levels between 4.1 and 5.5 mmol/L. Higher levels (> 5.5 mmol/L), on the other hand, were associated with cardiovascular events (or the composite endpoint of cardiovascular events or death). These observations may suggest the need for reevaluation of what constitutes a “normal range” for serum potassium in certain patient populations.[9] Potassium is the most abundant intracellular cation and about 98% of the body's potassium is found inside cells, with the remainder in the extracellular fluid including the blood. Membrane potential is maintained principally by the concentration gradient and membrane permeability to potassium with some contribution from the Na+/K+ pump. The potassium gradient is critically important for many physiological processes, including maintenance of cellular membrane potential, homeostasis of cell volume, and transmission of action potentials in nerve cells.[citation needed]
Its main dietary sources are vegetables (tomato and potato), fruits (orange and banana) and meat. Elimination is through the gastrointestinal tract, kidney and sweat glands. The renal elimination of potassium is passive (through the glomeruli), and reabsorption is active in the proximal tubule and the ascending limb of the loop of Henle. There is active excretion of potassium in the distal tubule and the collecting duct; both are controlled by aldosterone. In sweat glands potassium elimination is quite similar to the kidney, its excretion is also controlled by aldosterone.[citation needed]
Regulation of serum potassium is a function of intake, appropriate distribution between intracellular and extracellular compartments, and effective bodily excretion. In healthy individuals, homeostasis is maintained when cellular uptake and renal excretion naturally counterbalance a patient’s dietary intake of potassium.[10][11] When renal function becomes compromised, the ability of the body to effectively regulate serum potassium via the kidney declines. To compensate for this deficit in function, the colon increases its potassium secretion as part of an adaptive response. However, serum potassium will continue to be elevated as the colonic compensating mechanism reaches its limits.[12][13]
Hyperkalemia develops when there is excessive production (oral intake, tissue breakdown) or ineffective elimination of potassium. Ineffective elimination can be hormonal (in aldosterone deficiency) or due to causes in the renal parenchyma that impair excretion.[citation needed]
Increased extracellular potassium levels result in depolarization of the membrane potentials of cells due to the increase in the equilibrium potential of potassium. This depolarization opens some voltage-gated sodium channels, but also increases the inactivation at the same time. Since depolarization due to concentration change is slow, it never generates an action potential by itself instead, it results in accommodation. Above a certain level of potassium the depolarization inactivates sodium channels, opens potassium channels, thus the cells become refractory. This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems. Of most concern is the impairment of cardiac conduction which can result in ventricular fibrillation or asystole.[citation needed]
During extreme exercise, potassium is released from active muscle, and the serum potassium rises to a point that would be dangerous at rest. High levels of adrenaline and noradrenaline have a protective effect on the cardiac electrophysiology because they bind to beta 2 adrenergic receptors, which, when activated, extracellularly decrease potassium concentration.[14]
Patients with the rare hereditary condition of hyperkalemic periodic paralysis appear to have a heightened muscular sensitivity that is associated with transient elevation of potassium levels. Episodes of muscle weakness and spasms can be precipitated by exercise or fasting in these subjects.[citation needed]
Diagnosis
An ECG of a person with a potassium of 5.7 showing large T waves and small P waves
To gather enough information for diagnosis, the measurement of potassium needs to be repeated, as the elevation can be due to hemolysis in the first sample. The normal serum level of potassium is 3.5 to 5 mEq/L. Generally, blood tests for renal function (creatinine, blood urea nitrogen), glucose and occasionally creatine kinase and cortisol will be performed. Calculating the trans-tubular potassium gradient can sometimes help in distinguishing the cause of the hyperkalemia.[citation needed]
Also, electrocardiography (EKG/ECG) may be performed to determine if there is a significant risk of cardiac arrhythmias.[citation needed]
ECG findings
With mild to moderate hyperkalemia, there is reduction of the size of the P wave and development of peaked T waves. Severe hyperkalemia results in a widening of the QRS complex, and the ECG complex can evolve to a sinusoidal shape. There appears to be a direct effect of elevated potassium on some of the potassium channels that increases their activity and speeds membrane repolarization. Also, (as noted above), hyperkalemia causes an overall membrane depolarization that inactivates many sodium channels. The faster repolarization of the cardiac action potential causes the tenting of the T waves, and the inactivation of sodium channels causes a sluggish conduction of the electrical wave around the heart, which leads to smaller P waves and widening of the QRS complex.[citation needed]
The serum potassium concentration at which electrocardiographic changes develop is somewhat variable. Although the factors influencing the effect of serum potassium levels on cardiac electrophysiology are not entirely understood, the concentrations of other electrolytes, as well as levels of catecholamines, play a major role.[citation needed]
ECG findings are not a reliable finding in hyperkalemia. In retrospective review, blinded cardiologists documented peaked T-waves in only 3 of 90 ECGs with hyperkalemia. Sensitivity of peaked-Ts for hyperkalemia ranged from 0.18 to 0.52 depending on the criteria for peak-T waves.[citation needed]
Prevention
Preventing recurrence of hyperkalemia typically involves reduction of dietary potassium, removal of an offending medication, and/or the addition diuretic (such as furosemide or hydrochlorothiazide). Sodium polystyrene sulfonate and sorbital (combined as Kayexalate) are occasionally used on an ongoing basis to maintain lower serum levels of potassium. Concerns regarding its use are noted in the previous section.[citation needed]
Treatment
When arrhythmias occur, or when potassium levels exceed 6.5 mmol/l, emergency lowering of potassium levels is needed. Several agents are used to transiently lower K+ levels. Choice depends on the degree and cause of the hyperkalemia, and other aspects of the person's condition.
Myocardial excitability
Calcium (calcium chloride or calcium gluconate) increases threshold potential through a mechanism that is still unclear, thus restoring normal gradient between threshold potential and resting membrane potential, which is elevated abnormally in hyperkalemia. A standard ampule of 10% calcium chloride is 10 mL and contains 6.8 mmol of calcium. A standard ampule of 10% calcium gluconate is also 10 mL but has only 2.26 mmol of calcium. Clinical practice guidelines recommend giving 6.8 mmol for typical EKG findings of hyperkalemia. This is 10 mL of 10% calcium chloride or 30 mL of 10% calcium gluconate. Though calcium chloride is more concentrated, it is caustic to the veins and should only be given through a central line. Onset of action is less than five minutes and lasts about 30-60 min. The goal of treatment is to normalize the EKG and doses can be repeated if the EKG does not improve in 3 minutes.[citation needed]
Some textbooks suggest that calcium should not be given in digoxin toxicity as it has been linked to cardiovascular collapse in humans and increased digoxin toxicity in animal models. Recent literature questions if this is a real concern.[citation needed]
Temporary measures
Several medical treatments shift potassium ions from the bloodstream into the cellular compartment, thereby reducing the risk of complications. The effect of these measures tends to be short-lived, but may temporize the problem until potassium can be removed from the body.[15]
- Insulin (e.g. intravenous injection of 10-15 units of regular insulin along with 50 ml of 50% dextrose to prevent hypoglycemia) will lead to a shift of potassium ions into cells, secondary to increased activity of the sodium-potassium ATPase.[16] Its effects last a few hours, so it sometimes needs to be repeated while other measures are taken to suppress potassium levels more permanently. The insulin is usually given with an appropriate amount of glucose in order to prevent hypoglycemia following the insulin administration.
- Salbutamol (albuterol, Ventolin), a β2-selective catecholamine, is administered by nebulizer (e.g. 10–20 mg). This drug also lowers blood levels of K+ by promoting its movement into cells.[16]
- Though previously recommended, IV bicarbonate as a method to shift potassium into cells is no longer recommended. Not only has it not been effective in controlled trials[17] but it lowers ionized calcium levels, theoretically increasing the risk of cardiac arrhythmia.[citation needed]
Elimination
Severe cases require hemodialysis or hemofiltration, which are the most rapid methods of removing potassium from the body.[16] These are typically used if the underlying cause cannot be corrected swiftly while temporizing measures are instituted or there is no response to these measures.
Potassium can bind to agents throughout the gastrointestinal tract, where serum potassium is abundant in patients with renal impairment.[18][19] Potassium can be trapped by binding agents within the bowel. The only product approved by the FDA to treat hyperkalemia is sodium polystyrene sulfonate with sorbitol (Kayexalate), which can be given either orally or rectally to lower potassium over several hours.[16] Removal of potassium is assumed to require defecation. However, careful clinical trials to demonstrate the effectiveness of sodium polystyrene are lacking, and use of sodium polystyrene sulfonate, particularly if formulated with high sorbitol content, is uncommonly but convincingly associated with colonic necrosis.[20][21][22] There are no systematic studies (>6 months) looking at the long-term safety of this medication.[23]
Loop diuretics (Furosemide, bumetanide, torasemide) may can increase kidney potassium excretion in patients with intact kidney function.[16]
Fludrocortisone, a synthetic mineralocorticoid, can also increase renal potassium excretion in patients with functioning kidneys.[24][25] Trials of fludrocortisone in patients on dialysis have shown it to be ineffective.[26]
Research
ZS-9 is an investigational selective oral sorbent which traps potassium in the gastrointestinal tract.[27]
References
- ^ "High potassium (hyperkalemia) When to see a doctor - Symptoms". Mayo Clinic. 2011-11-18. Retrieved 2014-02-28.
- ^ "High potassium (hyperkalemia) Causes - Symptoms". Mayo Clinic. 2011-11-18. Retrieved 2014-02-28.
- ^ http://emedicine.medscape.com/article/154336-overview Retrieved 02-09-15
- ^ Su M, Stork C, Ravuri S, Lavoie T, Anguish D, Nelson LS, Hoffman RS; Stork; Ravuri; Lavoie; Anguish; Nelson; Hoffman (2001). "Sustained-release potassium chloride overdose". J. Toxicol. Clin. Toxicol. 39 (6): 641–8. doi:10.1081/CLT-100108499. PMID 11762675.
- ^ Sevastos N, Theodossiades G, Efstathiou S, Papatheodoridis GV, Manesis E, Archimandritis AJ; Theodossiades; Efstathiou; Papatheodoridis; Manesis; Archimandritis (March 2006). "Pseudohyperkalemia in serum: the phenomenon and its clinical magnitude". J. Lab. Clin. Med. 147 (3): 139–144. doi:10.1016/j.lab.2005.11.008. PMID 16503244.
- ^ Don BR, Sebastian A, Cheitlin M, Christiansen M, Schambelan M; Sebastian; Cheitlin; Christiansen; Schambelan (May 1990). "Pseudohyperkalemia caused by fist clenching during phlebotomy". N. Engl. J. Med. 322 (18): 1290–1292. doi:10.1056/NEJM199005033221806. PMID 2325722.
- ^ Iolascon A, Stewart GW, Ajetunmobi JF, Perrotta S, Delaunay J, Carella M, Zelante L, Gasparini P; Stewart; Ajetunmobi; Perrotta; Delaunay; Carella; Zelante; Gasparini (May 1999). "Familial pseudohyperkalemia maps to the same locus as dehydrated hereditary stomatocytosis (hereditary xerocytosis)". Blood 93 (9): 3120–3123. PMID 10216110.
- ^ Andolfo I, Alper SL, Delaunay J, Auriemma C, Russo R, Asci R, Esposito MR, Sharma AK, Shmukler BE, Brugnara C, De Franceschi L, Iolascon A; Alper; Delaunay; Auriemma; Russo; Asci; Esposito; Sharma; Shmukler; Brugnara; De Franceschi; Iolascon (January 2013). "Missense mutations in the ABCB6 transporter cause dominant familialpseudohyperkalemia". American Journal of Hematology 88 (1): 66–72. doi:10.1002/ajh.23357. PMID 23180570.
- ^ Korgaonkar, Sonal; Tilea, Anca; Gillespie, Brenda W.; Kiser, Margaret; Eisele, George; Finkelstein, Frederic; Kotanko, Peter; Pitt, Bertram; Saran, Rajiv. "Serum Potassium and Outcomes in CKD: Insights from the RRI-CKD Cohort Study". Clinical Journal of the American Society of Nephrology. pp. 762–769.
- ^ Brown, Robert (November 5, 1984). "Potassium Homeostasis and clinical implications". The American Journal of Medicine: 3–10. doi:10.1016/s0002-9343(84)80002-9.
- ^ Weiner, ID; Linas, SL; Wingo, CS (2010). Johnson, R.; Fluege, J.; Feehally, J., eds. Comprehensive Clinical Nephrology 4th ed. Chapter 9 Disorder of Potassium Metabolism: Saunders elsevier. pp. 118–129.
- ^ Mathialahan, T; Maclennan, KA; Sandle, LN; Verbeke, C; Sandle, GI (2005). "Enhanced large intestinal potassium permeability in end-stage renal disease". Journal of Pathology 206 (1): 46–51. doi:10.1002/path.1750. PMID 15772943.
- ^ Evans, KJ; Greenberg, A (2005). "Hyperkalemia: A review". J Intensive Care Med 20 (5): 272–290. doi:10.1177/0885066605278969. PMID 16145218.
- ^ Lindinger MI (April 1995). "Potassium regulation during exercise and recovery in humans: implications for skeletal and cardiac muscle". J. Mol. Cell. Cardiol. 27 (4): 1011–1022. doi:10.1016/0022-2828(95)90070-5. PMID 7563098.
- ^ Elliott MJ, Ronksley PE, Clase CM, Ahmed SB, Hemmelgarn BR; Ronksley; Clase; Ahmed; Hemmelgarn (October 2010). "Management of patients with acute hyperkalemia". CMAJ 182 (15): 1631–5. doi:10.1503/cmaj.100461. PMC 2952010. PMID 20855477.
- ^ a b c d e Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ, Jeejeebhoy FM, Gabrielli A; Morrison; Shuster; Donnino; Sinz; Lavonas; Jeejeebhoy; Gabrielli (2010-11-02). "Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care". Circulation 122 (18 Suppl 3): S829–61. doi:10.1161/CIRCULATIONAHA.110.971069. PMID 20956228.
- ^ Allon M, Shanklin N; Shanklin (Oct 1996). "Effect of bicarbonate administration on plasma potassium in dialysis patients: interactions with insulin and albuterol". American journal of kidney diseases : the official journal of the National Kidney Foundation 28 (4): 508–14. doi:10.1016/S0272-6386(96)90460-6. PMID 8840939.
- ^ HOLLANDER-RODRIGUEZ, JC; CALVERT, J (2006). "Hyperkalemia". Am Fam Physician 73 (2): 283–90. PMID 16445274.
- ^ Weiner, DI; Linas, SL; Wingo, CS (2010). Comprehensive Clinical Nephrology (4th ed.). Chapter 9: Disorders of potassium metabolism: Saunders Elsevier. pp. 118–129.
- ^ Watson M, Abbott KC, Yuan CM; Abbott; Yuan (2010). "Damned if You Do, Damned if You Don't: Potassium Binding Resins in Hyperkalemia". Clinical Journal of the American Society of Nephrology 5 (10): 1723–6. doi:10.2215/CJN.03700410. PMID 20798253.
- ^ Kamel KS, Schreiber M; Schreiber (2012). "Asking the question again: Are cation exchange resins effective for the treatment of hyperkalemia?". Nephrology Dialysis Transplantation 27 (12): 4294–7. doi:10.1093/ndt/gfs293. PMID 22989741.
- ^ Sterns RH, Rojas M, Bernstein P, Chennupati S; Rojas; Bernstein; Chennupati (May 2010). "Ion-exchange resins for the treatment of hyperkalemia: are they safe and effective?". J. Am. Soc. Nephrol. 21 (5): 733–5. doi:10.1681/ASN.2010010079. PMID 20167700.
- ^ Harel, Z; Harel, S; Shah, PS et al. (2013). "Gastrointestinal adverse events with sodium polystyrene sulfonate (kayexalate) use: a systematic review.". Am J Med 126 (264): e9–264.e24.
- ^ Sherman DS, Kass CL, Fish DN; Kass; Fish (May 2000). "Fludrocortisone for the treatment of heparin-induced hyperkalemia". The Annals of pharmacotherapy 34 (5): 606–10. doi:10.1345/aph.19326. PMID 10852087.
- ^ Dick TB, Raines AA, Stinson JB, Collingridge DS, Harmston GE; Raines; Stinson; Collingridge; Harmston (Sep 2011). "Fludrocortisone is effective in the management of tacrolimus-induced hyperkalemia in liver transplant recipients". Transplantation proceedings 43 (7): 2664–8. doi:10.1016/j.transproceed.2011.07.006. PMID 21911143.
- ^ Kaisar MO, Wiggins KJ, Sturtevant JM, Hawley CM, Campbell SB, Isbel NM, Mudge DW, Bofinger A, Petrie JJ, Johnson DW; Wiggins; Sturtevant; Hawley; Campbell; Isbel; Mudge; Bofinger; Petrie; Johnson (May 2006). "A randomized controlled trial of fludrocortisone for the treatment of hyperkalemia in hemodialysis patients". American journal of kidney diseases : the official journal of the National Kidney Foundation 47 (5): 809–14. doi:10.1053/j.ajkd.2006.01.014. PMID 16632019.
- ^ Worcester, S. "Novel agent appears safe, effective for hyperkalemia." Hospitalist News. December 18, 2013.[1]
External links
- USDA National Nutrient Database for Standard Reference, Release 26
- List of foods rich in potassium
- National Kidney Foundation site on potassium content of foods
|
Water-electrolyte imbalance and acid-base imbalance (E86–E87, 276)
|
|
| Volume status |
- Volume contraction (Dehydration/Hypovolemia)
- Hypervolemia
|
|
| Electrolyte |
| Na+ |
- Hypernatremia
- Hyponatremia (Hypotonic, Isotonic)
|
|
| K+ |
|
|
| Cl− |
- Hyperchloremia
- Hypochloremia
|
|
| Ca++ |
- Hypercalcaemia
- Hypocalcaemia
|
|
|
| Acid-base |
| Acidosis |
- Metabolic: High anion gap (Ketoacidosis/Diabetic ketoacidosis, Lactic)
- Normal anion gap (Hyperchloremic, Renal tubular)
|
|
| Alkalosis |
- Metabolic: Contraction alkalosis
|
|
| Both |
- Mixed disorder of acid-base balance
|
|
|
|
Index of the urinary system
|
|
| Description |
- Anatomy
- Physiology
- Development
- Cells
|
|
| Disease |
- Electrolyte and acid-base
- Congenital
- Neoplasms and cancer
- Other
- Symptoms and signs
- Urine tests
- Blood tests
|
|
| Treatment |
- Procedures
- Drugs
- Intravenous fluids
|
|
|
