Overview of acid-base

and electrolyte disorders

The right clinical information, right where it's needed

Last updated: Nov 27, 2018

 Table of Contents
Introduction 3

Conditions 4

References 10

Disclaimer 13
Overview of acid-base and electrolyte disorders Introduction

Introduction

INTRODUCTION
Disorders of blood chemistry may be caused by dietary factors, underlying medical conditions, and medical
treatments. Resulting imbalances include acidosis (pH <7.35), alkalosis (pH >7.45), and high or low levels
of key electrolyte ions, including sodium, potassium, calcium, magnesium, chloride, hydrogen phosphate,
and hydrogen carbonate (bicarbonate). They may be acute or chronic, may occur with varying degrees of
severity, and may not be sufficiently counteracted by the body's regulatory/compensatory mechanisms.

Electrolyte balance is normally regulated by the hypothalamus, kidneys, and various hormones, including
antidiuretic hormone (ADH), aldosterone (a mineralocorticoid hormone), and parathyroid hormone (PTH).
Acid-base balance is linked to fluid and electrolyte balance, and is normally controlled and maintained by
immediate buffer systems via the kidneys and the pulmonary system.[1] Respiratory acidosis and alkalosis
are accompanied by compensatory renal bicarbonate retention and loss, respectively; metabolic acidosis
and alkalosis are accompanied by compensatory hyperventilation and hypoventilation, respectively. Mixed
metabolic disorders can occur (e.g., diabetic ketoacidosis complicated by vomiting), and evaluation depends
on clinical history and examination, assessment of anion gap, serum electrolytes, and arterial blood gases.
These disorders can be effectively evaluated by a stepwise pathophysiological approach.[1] [2]

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 Overview of acid-base and electrolyte disorders Conditions

Conditions

◊ Assessment of respiratory acidosis

» see our comprehensive coverage of Assessment of respiratory acidosis
Respiratory acidosis occurs when arterial partial pressure levels of carbon dioxide (PCO₂) increase
to above the normal range of 4.7 to 6.0 kPa (35-45 mmHg), due to inefficient clearance of CO₂. This
leads to an accumulation of hydrogen ions, causing the arterial pH to fall below 7.35. It may be acute
or chronic, and failure to recognise and treat the underlying cause can lead to respiratory failure and
death. Acute respiratory acidosis (often life-threatening) is commonly caused by drug use (e.g., narcotics,
alcohol, sedatives, anaesthetics), oxygen therapy in COPD, head trauma, status asthmaticus, foreign
body aspiration, multilobar pneumonia, cardiogenic pulmonary oedema, pneumothorax, and inadequate
mechanical ventilation. Chronic respiratory acidosis is commonly caused by obesity (both hypoventilation
syndrome in obesity and impaired chest wall mobility) and COPD. Clinical features include respiratory
depression (hypoventilation), obtundation, haemodynamic instability, and respiratory muscle fatigue
CONDITIONS

(accessory muscle use, dyspnoea, tachypnoea).

◊ Assessment of respiratory alkalosis

» see our comprehensive coverage of Assessment of respiratory alkalosis
Respiratory alkalosis is an acid-base disorder characterised by a primary reduction of PCO₂ to below
the normal range of 4.7 to 6.0 kPa (35-45 mmHg), leading to an increase in pH to above 7.45 and a
subsequent decrease in bicarbonate from a normal value of 24 mmol/L (24 mEq/L). The decrease in
PCO₂ typically occurs as a result of alveolar hyperventilation with an excess of CO₂ excretion compared
to production.[3] The aetiologies of respiratory alkalosis are multiple and include hypoxia, parenchymal
lung disease, asthma, drug effects, mechanical ventilation, central nervous system disorders, metabolic
causes, pregnancy, and hyperventilation syndrome.[3] Respiratory alkalosis can be acute or chronic in
nature.

◊ Assessment of metabolic acidosis

» see our comprehensive coverage of Assessment of metabolic acidosis
Metabolic acidosis is indicated by an arterial pH of less than 7.35, a decrease in the plasma bicarbonate
level, and/or a marked increase in the serum anion gap (SAG; calculated by subtracting the sum of
major measured anions, chloride and bicarbonate, from the major measured cation, sodium). Where
SAG is normal (6-12 mmol/L [6-12 mEq/L]), gastrointestinal or renal causes are common.[4] This is also
referred to as hyperchloraemic or non-anion gap metabolic acidosis. Where SAG is increased, causes
include diabetic ketoacidosis, alcoholic ketoacidosis, lactic acidosis, kidney disease, or ingestion of
methanol, ethanol, ethylene glycol, propylene glycol, 5-oxoproline (e.g., in patients with chronic ingestion
of paracetamol), or salicylic acid. With simple metabolic acidosis, the normal adaptive respiratory
response will decrease the arterial PCO₂ 1.0 to 1.5 times the decrease in serum hydrogen carbonate
(bicarbonate).[5]

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Overview of acid-base and electrolyte disorders Conditions

◊ Assessment of metabolic alkalosis

» see our comprehensive coverage of Assessment of metabolic alkalosis
Metabolic alkalosis is an elevated arterial pH of above 7.45, and is the consequence of disorders
that cause either a loss of hydrogen ions from the body or an increase in plasma bicarbonate from a
normal value of 24 mmol/L (24 mEq/L). Causes include gastric secretion loss (e.g., vomiting, diarrhoea)
and mineralocorticoid excess. Patients may present with tingling, muscle cramps, weakness, cardiac
arrhythmias, and/or seizures.[6] [7] Some symptoms may be due to a decrease in circulating calcium,
which occurs when the pH is high. Patients may develop serious or fatal arrhythmias and/or seizures
without preceding symptoms. Compensatory metabolic alkalosis may be an incidental finding in patients
with chronic respiratory acidosis.

◊ Assessment of hyponatraemia
» see our comprehensive coverage of Assessment of hyponatraemia
Defined as a serum sodium <135 mmol/L (<135 mEq/L); severe hyponatraemia is defined as a serum
sodium <120 mmol/L (<120 mEq/L). Hyponatraemia is a common electrolyte disorder and is estimated
to occur in 15% of all hospital inpatients.[8] [9] With few exceptions, when the serum sodium level is

CONDITIONS
low, plasma osmolality is also low (hypotonic hyponatraemia). While defined by the level of sodium,
hypotonic hyponatraemia is, in fact, a disorder of water balance. Hyponatraemia is often iatrogenic and
avoidable. Common causes are administration of hypotonic fluids to patients and use of thiazide diuretics
(more likely to affect older people).[10] Hyponatraemia may also be a clue to the presence of serious
underlying medical disorders. Patients who develop hyponatraemia as a result of head injury, intracranial
surgery, subarachnoid haemorrhage, stroke, or brain tumours may have cerebral salt-wasting syndrome or
syndrome of inappropriate antidiuretic hormone (SIADH).

◊ Assessment of hypernatraemia
» see our comprehensive coverage of Assessment of hypernatraemia
Hypernatraemia is defined as a plasma sodium concentration of >145 mmol/L (>145 mEq/L).
Hypernatraemia is a state of hyperosmolality, and is primarily a result of water deficit or sodium gain.
Normally, persistently high sodium levels trigger antidiuretic hormone (ADH) release, stimulating thirst
mechanisms so that hypernatraemia rarely develops. Hospitalised patients often have impaired thirst
mechanisms, restricted access to water, and an increased risk of water loss (e.g., due to vomiting or
fever). They are also at risk for iatrogenic inadequate fluid replacement. Endocrine abnormalities such as
diabetes insipidus and mineralocorticoid excess may also lead to hypernatraemia.

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 Overview of acid-base and electrolyte disorders Conditions

◊ Assessment of hypokalaemia
» see our comprehensive coverage of Assessment of hypokalaemia
Hypokalaemia is a serum potassium level <3.5 mmol/L (<3.5 mEq/L). Clinical manifestations are typically
seen only if the serum potassium level is <3.0 mmol/L (<3.0 mEq/L), and include muscle weakness,
ECG changes, cardiac arrhythmias, rhabdomyolysis, and renal abnormalities. Hypokalaemia may
result from decreased potassium intake, increased potassium entry into cells, increased potassium
excretion (e.g., from the gastrointestinal tract, via urine or sweat), dialysis, or plasmapheresis. Possible
causes include chronic alcoholism, anorexia nervosa, hypocaloric protein diets for rapid weight loss,[11]
metabolic or respiratory alkalosis or renal tubular acidosis, hypothermia, vomiting, severe diarrhoea,[12]
primary aldosteronism, salt-wasting nephropathies, exercising in a hot climate,[13] cystic fibrosis,[14]
hypomagnesaemia, polyuria, hypokalaemic periodic paralysis, and burns and other dermatological
conditions. Some medicines can cause hypokalaemia, including diuretics, insulin treatment for diabetic
ketoacidosis or nonketotic hyperglycaemia, beta-adrenergic agonists such as salbutamol or terbutaline,
theophylline, chloroquine, laxative abuse or bowel-cleansing agent use, and administration of vitamin B12
or folic acid in megaloblastic anaemia.[12]

◊ Assessment of hyperkalaemia
CONDITIONS

» see our comprehensive coverage of Assessment of hyperkalaemia

Significant hyperkalemia is defined as a serum potassium value >6.0 mmol/L (>6.0 mEq/L). Moderate
hyperkalemia is defined as serum potassium values in the 5.0 to 6.0 mmol/L (5.0 to 6.0 mEq/L) range.
Hyperkalaemia can be life-threatening and may cause cardiac arrhythmias (ventricular fibrillation) by
affecting the cardiac action potential. Hyperkalaemia is often multifactorial in aetiology. It may result
from effective depletion of the circulating volume by heart failure combined with ACE inhibitors, or
from increased dietary potassium intake combined with chronic renal failure. It is essential to take a
thorough history of comorbidities and medicines that might increase cellular potassium release or
reduce urinary excretion. Reduced potassium excretion occurs in renal failure, volume depletion, and
hypoaldosteronism.[15] Dietary factors (e.g., excess consumption of foods high in potassium) or medicines
may quickly lead to hyperkalaemia in patients with comorbidities.

◊ Assessment of hypocalcaemia
» see our comprehensive coverage of Assessment of hypocalcaemia
Hypocalcaemia is a state of electrolyte imbalance in which the circulating serum calcium level is low.
Hypocalcaemia arises mainly from either insufficient entry of calcium into the circulation or an increased
loss of calcium from the circulation. Aetiologies include hypoparathyroidism, pseudohypoparathyroidism,
vitamin D deficiency, magnesium imbalance, hyperphosphataemia, hungry bone syndrome, acute
pancreatitis, extensive osteoblastic skeletal metastases, chelating agents (e.g., citrate, EDTA, lactate,
foscarnet), drug-induced, and use of gadolinium-based magnetic resonance imaging (MRI) contrast
agents. It is also seen in critically ill patients.

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Overview of acid-base and electrolyte disorders Conditions

◊ Assessment of hypercalcaemia
» see our comprehensive coverage of Assessment of hypercalcaemia
Symptoms from calcium elevation are typically not found unless the calcium is above 3 mmol/L (12 mg/
dL). Severe hypercalcaemia symptoms and coma are likely when calcium is >3.2 mmol/L (>13 mg/dL).
The most common causes of hypercalcaemia are primary hyperparathyroidism and malignancy (e.g.,
multiple myeloma, leukaemia, lung cancer, and breast cancer). Chronic symptoms are more consistent
with hyperparathyroidism, whereas recent onset of symptoms suggests malignancy (the tumour is typically
very advanced). Signs and symptoms include renal stones (typical of hyperparathyroidism), lethargy, easy
fatigue, depression, irritability, constipation, gastrointestinal symptoms (e.g., nausea, vomiting, abdominal
pain, peptic ulcer disease, pancreatitis), polyuria, polydipsia, increased risk of cardiac arrest (shortened
QT interval), confusion, and coma. Hypercalcaemia may be asymptomatic.[16]

◊ Assessment of magnesium deficiency

» see our comprehensive coverage of Assessment of magnesium deficiency
Hypomagnesaemia is defined as serum magnesium <0.9 mmol/L (<1.8 mEq/L). Magnesium deficiency

CONDITIONS
can be caused by decreased magnesium intake from the diet, decreased magnesium absorption, or
increased renal magnesium excretion (renal magnesium wasting). Symptoms are non-specific and include:
neuromuscular irritability similar to that produced by hypocalcaemia, manifesting with extensor plantar
reflexes, positive Trousseau's and Chvostek's signs, and, in severe cases, tetany; cardiovascular features
such as rapid heartbeats and an elevated blood pressure, tachycardia, and/or ventricular arrhythmias;
central nervous system symptoms of vertigo, ataxia, depression, and seizure activity.

◊ Primary hyperparathyroidism
» see our comprehensive coverage of Primary hyperparathyroidism
An endocrine disorder in which autonomous overproduction of parathyroid hormone (PTH) results
in calcium metabolism derangement. Single parathyroid adenomas are the most common aetiology
(approximately 80% of cases) and familial forms are also well defined.[17] Multiple adenomas and
hypertrophy of all 4 glands are less common. Diagnosis occurs through testing for a concurrent elevated
serum calcium level and an inappropriately elevated intact serum PTH level. Inherited forms, affecting
10% to 20% of patients,[18] lead to hyperfunctioning parathyroid glands. Importantly, <1% of cases
of hyperparathyroidism are caused by parathyroid carcinoma. Complications due to primary PTH are
uncommon and include osteoporosis and bone fracture due to leaching of calcium from bones, and renal
calculi due to elevated serum and urine calcium. In 2017, normocalcaemic primary hyperparathyroidism
was recognised as a variant of primary hyperparathyroidism and has yet to be thoroughly characterised.

◊ Diabetic ketoacidosis
» see our comprehensive coverage of Diabetic ketoacidosis
Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes that is potentially fatal and
requires prompt medical attention for successful treatment. DKA may be the initial presentation in people
with newly diagnosed diabetes. It is usually characterised by plasma glucose >13.9 mmol/L (>250 mg/
dL), arterial pH 7.0 to <7.3, and the presence of ketonaemia and/or ketonuria. Serum sodium, chloride,
magnesium, and calcium are usually low, and serum anion gap (SAG; calculated by subtracting the sum
of major measured anions, chloride and bicarbonate, from the major measured cation, sodium), serum
potassium, urea, and creatinine are usually elevated. Arterial bicarbonate ranges from <10 mmol/L (<10
mEq/L) in severe DKA to >15 mmol/L (>15 mEq/L) in mild DKA. Venous pH, which is usually 0.03 units
lower than arterial pH, is recommended for monitoring treatment, but the difference should be noted.

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 Overview of acid-base and electrolyte disorders Conditions

◊ Hyperosmolar hyperglycaemic state

» see our comprehensive coverage of Hyperosmolar hyperglycaemic state
A serious metabolic complication of diabetes characterised by profound hyperglycaemia (glucose >33
mmol/L [>600 mg/dL]), hyperosmolality (effective serum osmolality >320 mmol/kg [>320 mOsm/kg]),
and volume depletion in the absence of significant ketoacidosis (pH >7.3 and hydrogen carbonate
[bicarbonate] >15 mmol/L [>15 mEq/L]).[19] It is most common in older patients with type 2 diabetes.
Infection is the major precipitating factor, occurring in 30% to 60% of patients. Urinary tract infections and
pneumonia are the most common infections reported.[19] [20]

◊ Renal tubular acidosis

» see our comprehensive coverage of Renal tubular acidosis
The term 'renal tubular acidosis' (RTA) describes any one of a number of disorders in which the excretion
of fixed acid (distal RTA) or the reabsorption of filtered bicarbonate (proximal RTA) is impaired to a degree
disproportionate to any existing impairment of the glomerular filtration rate.[21] The acid retention or
bicarbonate loss results in the development of hyperchloraemic metabolic acidosis marked by low serum
bicarbonate and arterial blood pH. In the absence of other acid-base disorders the serum anion gap
CONDITIONS

(SAG; calculated by subtracting the sum of major measured anions, chloride and bicarbonate, from
the major measured cation, sodium) is normal. Proximal and classic distal RTA are characterised by
hypokalaemia.[21] [22] Hyperkalaemia in distal RTA indicates that aldosterone deficiency or resistance is
the cause of the problem.[22] There is minimal or absent urine ammonium in hyperkalaemic distal RTA.
Serum sodium is usually normal. RTA is rarely symptomatic. Patients with severe acidaemia can show
hyperventilation or Kussmaul's breathing due to respiratory compensation. The urine pH exceeds 5.5 in
classic distal RTA, but is lower than 5.0 in patients with untreated proximal RTA.

◊ Primary aldosteronism
» see our comprehensive coverage of Primary aldosteronism
In primary aldosteronism (PA), aldosterone production exceeds the body's requirements and is relatively
autonomous with regard to its normal chronic regulator, the renin-angiotensin II (AII) system.[23] [24] This
results in excessive sodium reabsorption via amiloride-sensitive epithelial sodium channels within the distal
nephron, leading to hypertension and suppression of renin-AII. Urinary loss of potassium and hydrogen
ions, exchanged for sodium at the distal nephron, may result in hypokalaemia and metabolic alkalosis
if severe and prolonged.[23] [24] This is the most common specifically treatable and potentially curable
form of hypertension, accounting for at least 5% of hypertensive patients.[25] Most of these patients are
normokalaemic.

◊ Addison's disease
» see our comprehensive coverage of Addison's disease
Primary adrenal insufficiency, or Addison's disease, is a disorder that affects the adrenal glands, causing
decreased production of adrenocortical hormones (cortisol, aldosterone, and dehydroepiandrosterone).
This may be caused by a destructive process directly affecting the adrenal glands or a condition that
interferes with hormone synthesis. Approximately 90% of the adrenal cortex needs to be destroyed
to produce adrenal insufficiency. Addison's disease may be either acute (adrenal crisis) or insidious.
The finding of low sodium and high potassium serum levels is typical. If untreated, it is a potentially life-
threatening condition.

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Overview of acid-base and electrolyte disorders Conditions

◊ Syndrome of inappropriate antidiuretic hormone

» see our comprehensive coverage of Syndrome of inappropriate antidiuretic hormone
Arginine vasopressin (AVP), also known as antidiuretic hormone (ADH), facilitates free water absorption in
the collecting tubule. Inappropriate secretion is characterised by hypotonic hyponatraemia, concentrated
urine, and a euvolaemic state. It is primarily identified by abnormal serum sodium levels on laboratory
testing, but patients may present with signs of cerebral oedema, including nausea, vomiting, headache,
mental status changes, increased somnolence, or coma, and appear euvolaemic.

CONDITIONS

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 Overview of acid-base and electrolyte disorders References

Key articles
• Berend K, de Vries AP, Gans RO. Physiological approach to assessment of acid-base disturbances. N
REFERENCES

Engl J Med. 2014 Oct 9;371(15):1434-45. Abstract

• Seifter JL. Integration of acid-base and electrolyte disorders. N Engl J Med. 2014 Nov
6;371(19):1821-31. Abstract

• Foster GT, Varizi ND, Sassoon CS. Respiratory alkalosis. Respir Care. 2001 Apr;46(4):384-91.
Abstract

• Spasovski G, Vanholder R, Allolio B, et al. Clinical practice guideline on diagnosis and treatment of
hyponatraemia. Eur J Endocrinol. 2014 Feb 25;170(3):G1-47. Full text Abstract

• Wakil A, Ng JM, Atkin SL. Investigating hyponatraemia. BMJ. 2011 Mar 7;342:d1118. Abstract

• Kitabchi AE, Umpierrez GE, Miles JM, et al. Hyperglycemic crises in adult patients with diabetes.
Diabetes Care. 2009 Jul;32(7):1335-43. Full text Abstract

• Batlle D, Moorthi KM, Schluter W, et al. Distal renal tubular acidosis and the potassium enigma. Semin
Nephrol. 2006 Nov;26(6):471-8. Abstract

References
1. Berend K, de Vries AP, Gans RO. Physiological approach to assessment of acid-base disturbances. N
Engl J Med. 2014 Oct 9;371(15):1434-45. Abstract

2. Seifter JL. Integration of acid-base and electrolyte disorders. N Engl J Med. 2014 Nov
6;371(19):1821-31. Abstract

3. Foster GT, Varizi ND, Sassoon CS. Respiratory alkalosis. Respir Care. 2001 Apr;46(4):384-91.
Abstract

4. Batlle DC, Hizon M, Cohen E, et al. The use of urinary anion gap in the diagnosis of hyperchloremic
metabolic acidosis. N Engl J Med. 1988 Mar 10;318(10):594-9. Abstract

5. Fencl V, Miller TB, Pappenheimer JR. Studies on respiratory response to disturbances of acid-base
balance, with deductions concerning the ionic composition of cerebral interstitial fluid. Am J Physiol.
1966 Mar;210(3):459-72. Abstract

6. Miller RB. Central nervous system manifestation of fluid and electrolyte disturbances. Surg Clin North
Am. 1968 Apr;48(2):381-93. Abstract

7. Morrison RS. Management of emergencies: metabolic acidosis and alkalosis. N Engl J Med. 1966 May
26;274(21):1195-7. Abstract

10 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 27, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
Overview of acid-base and electrolyte disorders References
8. Spasovski G, Vanholder R, Allolio B, et al. Clinical practice guideline on diagnosis and treatment of
hyponatraemia. Eur J Endocrinol. 2014 Feb 25;170(3):G1-47. Full text Abstract

REFERENCES
9. Mohan S, Gu S, Parikh A, et al. Prevalence of hyponatremia and association with mortality: results
from NHANES. Am J Med. 2013 Dec;126(12):1127-37.e1. Full text Abstract

10. Wakil A, Ng JM, Atkin SL. Investigating hyponatraemia. BMJ. 2011 Mar 7;342:d1118. Abstract

11. Liu T, Nagami GT, Everett ML, et al. Very low calorie diets and hypokalaemia: the importance of
ammonium excretion. Nephrol Dial Transplant. 2005 Mar;20(3):642-6. Full text Abstract

12. Rose BD, Post TW. Clinical physiology of acid-base and electrolyte disorders. 5th ed. New York, NY:
McGraw-Hill; 2001:836-56.

13. Godek SF, Godek JJ, Bartolozzi AR. Hydration status in college football players during consecutive
days of twice-a-day preseason practices. Am J Sports Med. 2005 Jun;33(6):843-51. Abstract

14. Dave S, Honney S, Raymond J, et al. An unusual presentation of cystic fibrosis in an adult. Am J
Kidney Dis. 2005 Mar;45(3):e41-4. Abstract

15. Hollander-Rodriguez JC, Calvert JF. Hyperkalemia. Am Fam Physician. 2006 Jan 15;73(2):283-90.
Full text Abstract

16. Bilezikian JP, Potts JT Jr, Fuleihan G el-H, et al. Summary statement from a workshop on
asymptomatic primary hyperparathyroidism: a perspective for the 21st century. J Clin Endocrinol
Metab. 2002 Dec;87(12):5353-61. Full text Abstract

17. Arnold A, Staunton CE, Kim HG, et al. Monoclonality and abnormal parathyroid hormone genes in
parathyroid adenomas. N Engl J Med. 1988 Mar 17;318(11):658-62. Abstract

18. Farford B, Presutti RJ, Moraghan TJ. Nonsurgical management of primary hyperparathyroidism. Mayo
Clin Proc. 2007 Mar;82(3):351-5. [Erratum in: Mayo Clin Proc. 2007 Jul;82(7):890.] Abstract

19. Kitabchi AE, Umpierrez GE, Miles JM, et al. Hyperglycemic crises in adult patients with diabetes.
Diabetes Care. 2009 Jul;32(7):1335-43. Full text Abstract

20. Trence DL, Hirsch IB. Hyperglycemic crises in diabetes mellitus type 2. Endocrinol Metab Clin North
Am. 2001 Dec;30(4):817-31. Abstract

21. Batlle D, Moorthi KM, Schluter W, et al. Distal renal tubular acidosis and the potassium enigma. Semin
Nephrol. 2006 Nov;26(6):471-8. Abstract

22. Rodriguez Soriano J. Renal tubular acidosis: the clinical entity. J Am Soc Nephrol. 2002
Aug;13(8):2160-70. Full text Abstract

23. Conn JW. Primary aldosteronism, a new clinical syndrome. J Lab Clin Med. 1955;45:6-17.

24. Conn JW. Plasma renin activity in primary aldosteronism. Importance in differential diagnosis and in
research of essential hypertension. JAMA. 1964 Oct 19;190:222-5. Abstract

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 27, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
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of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 Overview of acid-base and electrolyte disorders References
25. Morillas P, Castillo J, Quiles J, et al. Prevalence of primary aldosteronism in hypertensive patients and
its effect on the heart [in Spanish]. Rev Esp Cardiol. 2008 Apr;61(4):418-21. Abstract
REFERENCES

12 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: Nov 27, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
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Overview of acid-base and electrolyte disorders Disclaimer

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Contributors:

// Authors:

Editorial Team,
BMJ Publishing Group
DISCLOSURES: This overview has been compiled using the information in existing sub-topics.