Hyperkalemia differential diagnosis: Difference between revisions

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Revision as of 14:55, 16 July 2018

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Overview

Hyperkalemia is a laboratory finding that is a result of several conditions. These conditions must be differentiated as a cause of hyperkalemia. The following table summarize the differentiating features of causes of hyperkalemia.

Differential Diagnosis

Hyperkalemia is a laboratory finding that is a result of several conditions. These conditions must be differentiated as a cause of hyperkalemia. The following table summarize the differentiating features of causes of hyperkalemia

Organ system	Conditions	Distinguishing features			Additional findings
Organ system	Conditions	Symptoms	Signs	Labs	Additional findings
Renal	Acute kidney injury^[1]	Nausea, vomiting, decreased urine output, fatigue, dyspnea, edema	Tremor, confusion, edema	Hyperkalemia, increased BUN and Cr, metabolic acidosis	Recently developed symptoms
	Chronic kidney disease^[2]	Nausea, vomiting, decreased urine output, fatigue, dyspnea, edema	Tremor, confusion, edema	Hyperkalemia, increased BUN and Cr, metabolic acidosis, hypocalcemia, hyperphosphatemia	Chronic underlying disease (DM, HTN), duration of symptoms ≥ 3 months
	Renal tubular acidosis type-4^[3]	Usually asyptomatic	Signs of underlying disease	Hyperkalemia, normal anion gap metabolic acidosis, urine PH< 5.5	History of diabetes mellitus
Endocrine	DKA^[4]	Change in mental status, abdominal pain	Decreased skin turgor, dry oral mucosa, tachycardia	Hyperglycemia, increased anion gap metabolic acidosis, ketonemia	Rapidly developing polyuria, polydipsia, and weight loss
	HHS^[5]	Change in mental status, abdominal pain	Decreased skin turgor, dry oral mucosa, tachycardia	Severe hyperglycemia, normal anion gap, increased serum osmolality	Polyuria, polydipsia, and weight loss develop more insidious
	Congenital adrenal hyperplasia (CAH)^[6]^[7]	Poor feeding, failure to thrive, precocious puberty, short statue, hirsutism, weight loss	Ambiguous genitalia, hypotension	Hyperkalemia, increased 17 hydroxyprogestrone, hyponatremia	Salt wasting
	Addison's disease	Skin hyperpigmentation, fatigue, salt craving, nausea and vomiting, amenorrhea, depression	Hyperpigmentation, hypotension, pubic and axillary hair loss	Hyperkalemia, decreased serum cortisol level	Diagnosis by cosyntropin test
Tissue break down	Tumor lysis syndrome^[8]	Fever, weight loss, symptoms related to underlying malignancy	Altered mental status, lymphadenopathy, muscle weakness	Hyperkalemia, hyperphosphatemia, hypocalcemia	History of underlying malignancy
Tissue break down	Rhabdomyolysis^[9]	Myalgia, fatigue	Altered mental status, hypotension	Hyperkalemia, increased muscle enzymes (CK, aldolase)	History of seizure, drug overdose, or trauma

References

↑ Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, Levin A (2007). "Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury". Crit Care. 11 (2): R31. doi:10.1186/cc5713. PMC 2206446. PMID 17331245.
↑ Rodríguez Soriano J (2002). "Renal tubular acidosis: the clinical entity". J. Am. Soc. Nephrol. 13 (8): 2160–70. PMID 12138150.
↑ Hsu CY, Vittinghoff E, Lin F, Shlipak MG (2004). "The incidence of end-stage renal disease is increasing faster than the prevalence of chronic renal insufficiency". Ann. Intern. Med. 141 (2): 95–101. PMID 15262664.
↑ Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN (2009). "Hyperglycemic crises in adult patients with diabetes". Diabetes Care. 32 (7): 1335–43. doi:10.2337/dc09-9032. PMC 2699725. PMID 19564476.
↑ Arieff AI, Carroll HJ (1972). "Nonketotic hyperosmolar coma with hyperglycemia: clinical features, pathophysiology, renal function, acid-base balance, plasma-cerebrospinal fluid equilibria and the effects of therapy in 37 cases". Medicine (Baltimore). 51 (2): 73–94. PMID 5013637.
↑ Speiser PW, Azziz R, Baskin LS, Ghizzoni L, Hensle TW, Merke DP, Meyer-Bahlburg HF, Miller WL, Montori VM, Oberfield SE, Ritzen M, White PC (2010). "Congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency: an Endocrine Society clinical practice guideline". J. Clin. Endocrinol. Metab. 95 (9): 4133–60. doi:10.1210/jc.2009-2631. PMC 2936060. PMID 20823466.
↑ Hahner S, Loeffler M, Bleicken B, Drechsler C, Milovanovic D, Fassnacht M, Ventz M, Quinkler M, Allolio B (2010). "Epidemiology of adrenal crisis in chronic adrenal insufficiency: the need for new prevention strategies". Eur. J. Endocrinol. 162 (3): 597–602. doi:10.1530/EJE-09-0884. PMID 19955259.
↑ Coiffier B, Altman A, Pui CH, Younes A, Cairo MS (2008). "Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review". J. Clin. Oncol. 26 (16): 2767–78. doi:10.1200/JCO.2007.15.0177. PMID 18509186.
↑ Knochel JP (1982). "Rhabdomyolysis and myoglobinuria". Annu. Rev. Med. 33: 435–43. doi:10.1146/annurev.me.33.020182.002251. PMID 6282181.

Template:WikiDoc Sources

[pmid17331245-1] Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, Levin A (2007). "Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury". Crit Care. 11 (2): R31. doi:10.1186/cc5713. PMC 2206446. PMID 17331245.

[pmid12138150-2] Rodríguez Soriano J (2002). "Renal tubular acidosis: the clinical entity". J. Am. Soc. Nephrol. 13 (8): 2160–70. PMID 12138150.

[pmid15262664-3] Hsu CY, Vittinghoff E, Lin F, Shlipak MG (2004). "The incidence of end-stage renal disease is increasing faster than the prevalence of chronic renal insufficiency". Ann. Intern. Med. 141 (2): 95–101. PMID 15262664.

[pmid19564476-4] Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN (2009). "Hyperglycemic crises in adult patients with diabetes". Diabetes Care. 32 (7): 1335–43. doi:10.2337/dc09-9032. PMC 2699725. PMID 19564476.

[pmid5013637-5] Arieff AI, Carroll HJ (1972). "Nonketotic hyperosmolar coma with hyperglycemia: clinical features, pathophysiology, renal function, acid-base balance, plasma-cerebrospinal fluid equilibria and the effects of therapy in 37 cases". Medicine (Baltimore). 51 (2): 73–94. PMID 5013637.

[pmid20823466-6] Speiser PW, Azziz R, Baskin LS, Ghizzoni L, Hensle TW, Merke DP, Meyer-Bahlburg HF, Miller WL, Montori VM, Oberfield SE, Ritzen M, White PC (2010). "Congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency: an Endocrine Society clinical practice guideline". J. Clin. Endocrinol. Metab. 95 (9): 4133–60. doi:10.1210/jc.2009-2631. PMC 2936060. PMID 20823466.

[pmid19955259-7] Hahner S, Loeffler M, Bleicken B, Drechsler C, Milovanovic D, Fassnacht M, Ventz M, Quinkler M, Allolio B (2010). "Epidemiology of adrenal crisis in chronic adrenal insufficiency: the need for new prevention strategies". Eur. J. Endocrinol. 162 (3): 597–602. doi:10.1530/EJE-09-0884. PMID 19955259.

[pmid18509186-8] Coiffier B, Altman A, Pui CH, Younes A, Cairo MS (2008). "Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review". J. Clin. Oncol. 26 (16): 2767–78. doi:10.1200/JCO.2007.15.0177. PMID 18509186.

[pmid6282181-9] Knochel JP (1982). "Rhabdomyolysis and myoglobinuria". Annu. Rev. Med. 33: 435–43. doi:10.1146/annurev.me.33.020182.002251. PMID 6282181.

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 ==Overview==
 Hyperkalemia is a laboratory finding that is a result of several conditions. These conditions must be differentiated as a cause of hyperkalemia. The following table summarize the differentiating features of causes of hyperkalemia.
@@ Line 13: / Line 13: @@
 Hyperkalemia is a laboratory finding that is a result of several conditions. These conditions must be differentiated as a cause of hyperkalemia. The following table summarize the differentiating features of causes of hyperkalemia<br>
 <br>
-{| align=center
+{| align="center"
 |-
 |
-{| style="border: 0px; font-size: 90%; margin: 3px;" align=center
+{| style="border: 0px; font-size: 90%; margin: 3px;" align="center"
-! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" |Organ system
+! style="background:#4479BA; color: #FFFFFF;" align="center" rowspan="2" |Organ system
-! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" |Conditions
+! style="background:#4479BA; color: #FFFFFF;" align="center" rowspan="2" |Conditions
-! colspan="3" align="center" style="background:#4479BA; color: #FFFFFF;" |Distinguishing features
+! style="background:#4479BA; color: #FFFFFF;" colspan="3" align="center" |Distinguishing features
-! rowspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" |Additional findings
+! style="background:#4479BA; color: #FFFFFF;" align="center" rowspan="2" |Additional findings
 |-
-!align="center" style="background:#4479BA; color: #FFFFFF;" |Symptoms
+! style="background:#4479BA; color: #FFFFFF;" align="center" |Symptoms
-!align="center" style="background:#4479BA; color: #FFFFFF;" |Signs
+! style="background:#4479BA; color: #FFFFFF;" align="center" |Signs
-!align="center" style="background:#4479BA; color: #FFFFFF;" |Labs
+! style="background:#4479BA; color: #FFFFFF;" align="center" |Labs
 |-
-| rowspan="3" align="center" style="background:#DCDCDC;"|Renal
+| style="background:#DCDCDC;" align="center" rowspan="3" |Renal
-|align="center" style="background:#DCDCDC;"|Acute kidney injury<ref name="pmid17331245">{{cite journal |vauthors=Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, Levin A |title=Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury |journal=Crit Care |volume=11 |issue=2 |pages=R31 |year=2007 |pmid=17331245 |pmc=2206446 |doi=10.1186/cc5713 |url=}}</ref>
+| style="background:#DCDCDC;" align="center" |Acute kidney injury<ref name="pmid17331245">{{cite journal |vauthors=Mehta RL, Kellum JA, Shah SV, Molitoris BA, Ronco C, Warnock DG, Levin A |title=Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury |journal=Crit Care |volume=11 |issue=2 |pages=R31 |year=2007 |pmid=17331245 |pmc=2206446 |doi=10.1186/cc5713 |url=}}</ref>
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Nausea]], [[vomiting]], decreased [[urine output]], [[fatigue]], [[dyspnea]], [[edema]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Nausea]], [[vomiting]], decreased [[urine output]], [[fatigue]], [[dyspnea]], [[edema]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Tremor]], [[confusion]], [[edema]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Tremor]], [[confusion]], [[edema]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperkalemia]], [[Azotemia|increased BUN and Cr]], [[metabolic acidosis]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperkalemia]], [[Azotemia|increased BUN and Cr]], [[metabolic acidosis]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Recently developed symptoms
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Recently developed symptoms
 |-
-|align="center" style="background:#DCDCDC;"|Chronic kidney disease<ref name="pmid12138150">{{cite journal |vauthors=Rodríguez Soriano J |title=Renal tubular acidosis: the clinical entity |journal=J. Am. Soc. Nephrol. |volume=13 |issue=8 |pages=2160–70 |year=2002 |pmid=12138150 |doi= |url=}}</ref>
+| style="background:#DCDCDC;" align="center" |Chronic kidney disease<ref name="pmid12138150">{{cite journal |vauthors=Rodríguez Soriano J |title=Renal tubular acidosis: the clinical entity |journal=J. Am. Soc. Nephrol. |volume=13 |issue=8 |pages=2160–70 |year=2002 |pmid=12138150 |doi= |url=}}</ref>
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Nausea]], [[vomiting]], decreased [[urine output]], [[fatigue]], [[dyspnea]], [[edema]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Nausea]], [[vomiting]], decreased [[urine output]], [[fatigue]], [[dyspnea]], [[edema]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Tremor]], [[confusion]], [[edema]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Tremor]], [[confusion]], [[edema]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperkalemia]], [[Azotemia|increased BUN and Cr]], [[metabolic acidosis]], [[hypocalcemia]], [[hyperphosphatemia]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperkalemia]], [[Azotemia|increased BUN and Cr]], [[metabolic acidosis]], [[hypocalcemia]], [[hyperphosphatemia]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Chronic underlying disease ([[Diabetes mellitus|DM]], [[Hypertension|HTN]]), duration of symptoms ≥ 3 months
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Chronic underlying disease ([[Diabetes mellitus|DM]], [[Hypertension|HTN]]), duration of symptoms ≥ 3 months
 |-
-|align="center" style="background:#DCDCDC;"|[[Renal tubular acidosis|Renal tubular acidosis type-4]]<ref name="pmid15262664">{{cite journal |vauthors=Hsu CY, Vittinghoff E, Lin F, Shlipak MG |title=The incidence of end-stage renal disease is increasing faster than the prevalence of chronic renal insufficiency |journal=Ann. Intern. Med. |volume=141 |issue=2 |pages=95–101 |year=2004 |pmid=15262664 |doi= |url=}}</ref>
+| style="background:#DCDCDC;" align="center" |[[Renal tubular acidosis|Renal tubular acidosis type-4]]<ref name="pmid15262664">{{cite journal |vauthors=Hsu CY, Vittinghoff E, Lin F, Shlipak MG |title=The incidence of end-stage renal disease is increasing faster than the prevalence of chronic renal insufficiency |journal=Ann. Intern. Med. |volume=141 |issue=2 |pages=95–101 |year=2004 |pmid=15262664 |doi= |url=}}</ref>
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Usually asyptomatic
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Usually asyptomatic
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Signs of underlying disease
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Signs of underlying disease
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperkalemia]], normal anion gap metabolic acidosis, urine PH< 5.5
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperkalemia]], normal anion gap metabolic acidosis, urine PH< 5.5
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |History of [[diabetes mellitus]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |History of [[diabetes mellitus]]
 |-
-| rowspan="4" align="center" style="background:#DCDCDC;"|Endocrine
+| style="background:#DCDCDC;" align="center" rowspan="4" |Endocrine
-|align="center" style="background:#DCDCDC;"|[[Diabetic ketoacidosis|DKA]]<ref name="pmid19564476">{{cite journal |vauthors=Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN |title=Hyperglycemic crises in adult patients with diabetes |journal=Diabetes Care |volume=32 |issue=7 |pages=1335–43 |year=2009 |pmid=19564476 |pmc=2699725 |doi=10.2337/dc09-9032 |url=}}</ref>
+| style="background:#DCDCDC;" align="center" |[[Diabetic ketoacidosis|DKA]]<ref name="pmid19564476">{{cite journal |vauthors=Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN |title=Hyperglycemic crises in adult patients with diabetes |journal=Diabetes Care |volume=32 |issue=7 |pages=1335–43 |year=2009 |pmid=19564476 |pmc=2699725 |doi=10.2337/dc09-9032 |url=}}</ref>
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Change in mental status]], [[abdominal pain]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Change in mental status]], [[abdominal pain]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Decreased skin turgor, dry oral mucosa, [[tachycardia]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Decreased skin turgor, dry oral mucosa, [[tachycardia]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperglycemia]], increased anion gap [[metabolic acidosis]], [[ketonemia]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperglycemia]], increased anion gap [[metabolic acidosis]], [[ketonemia]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Rapidly developing [[polyuria]], [[polydipsia]], and [[weight loss]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Rapidly developing [[polyuria]], [[polydipsia]], and [[weight loss]]
 |-
-|align="center" style="background:#DCDCDC;"|[[Hyperosmolar hyperglycemic state|HHS]]<ref name="pmid5013637">{{cite journal |vauthors=Arieff AI, Carroll HJ |title=Nonketotic hyperosmolar coma with hyperglycemia: clinical features, pathophysiology, renal function, acid-base balance, plasma-cerebrospinal fluid equilibria and the effects of therapy in 37 cases |journal=Medicine (Baltimore) |volume=51 |issue=2 |pages=73–94 |year=1972 |pmid=5013637 |doi= |url=}}</ref>
+| style="background:#DCDCDC;" align="center" |[[Hyperosmolar hyperglycemic state|HHS]]<ref name="pmid5013637">{{cite journal |vauthors=Arieff AI, Carroll HJ |title=Nonketotic hyperosmolar coma with hyperglycemia: clinical features, pathophysiology, renal function, acid-base balance, plasma-cerebrospinal fluid equilibria and the effects of therapy in 37 cases |journal=Medicine (Baltimore) |volume=51 |issue=2 |pages=73–94 |year=1972 |pmid=5013637 |doi= |url=}}</ref>
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Change in mental status]], [[abdominal pain]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Change in mental status]], [[abdominal pain]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Decreased skin turgor, dry oral mucosa, [[tachycardia]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Decreased skin turgor, dry oral mucosa, [[tachycardia]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Severe [[hyperglycemia]], normal anion gap, increased serum osmolality
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Severe [[hyperglycemia]], normal anion gap, increased serum osmolality
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Polyuria]], [[polydipsia]], and [[weight loss]] develop more insidious
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Polyuria]], [[polydipsia]], and [[weight loss]] develop more insidious
 |-
-|align="center" style="background:#DCDCDC;"|[[Congenital adrenal hyperplasia]] (CAH)<ref name="pmid20823466">{{cite journal |vauthors=Speiser PW, Azziz R, Baskin LS, Ghizzoni L, Hensle TW, Merke DP, Meyer-Bahlburg HF, Miller WL, Montori VM, Oberfield SE, Ritzen M, White PC |title=Congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency: an Endocrine Society clinical practice guideline |journal=J. Clin. Endocrinol. Metab. |volume=95 |issue=9 |pages=4133–60 |year=2010 |pmid=20823466 |pmc=2936060 |doi=10.1210/jc.2009-2631 |url=}}</ref><ref name="pmid19955259">{{cite journal |vauthors=Hahner S, Loeffler M, Bleicken B, Drechsler C, Milovanovic D, Fassnacht M, Ventz M, Quinkler M, Allolio B |title=Epidemiology of adrenal crisis in chronic adrenal insufficiency: the need for new prevention strategies |journal=Eur. J. Endocrinol. |volume=162 |issue=3 |pages=597–602 |year=2010 |pmid=19955259 |doi=10.1530/EJE-09-0884 |url=}}</ref>
+| style="background:#DCDCDC;" align="center" |[[Congenital adrenal hyperplasia]] (CAH)<ref name="pmid20823466">{{cite journal |vauthors=Speiser PW, Azziz R, Baskin LS, Ghizzoni L, Hensle TW, Merke DP, Meyer-Bahlburg HF, Miller WL, Montori VM, Oberfield SE, Ritzen M, White PC |title=Congenital adrenal hyperplasia due to steroid 21-hydroxylase deficiency: an Endocrine Society clinical practice guideline |journal=J. Clin. Endocrinol. Metab. |volume=95 |issue=9 |pages=4133–60 |year=2010 |pmid=20823466 |pmc=2936060 |doi=10.1210/jc.2009-2631 |url=}}</ref><ref name="pmid19955259">{{cite journal |vauthors=Hahner S, Loeffler M, Bleicken B, Drechsler C, Milovanovic D, Fassnacht M, Ventz M, Quinkler M, Allolio B |title=Epidemiology of adrenal crisis in chronic adrenal insufficiency: the need for new prevention strategies |journal=Eur. J. Endocrinol. |volume=162 |issue=3 |pages=597–602 |year=2010 |pmid=19955259 |doi=10.1530/EJE-09-0884 |url=}}</ref>
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Poor feeding]], [[failure to thrive]], [[precocious puberty]], short statue, [[hirsutism]], [[weight loss]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Poor feeding]], [[failure to thrive]], [[precocious puberty]], short statue, [[hirsutism]], [[weight loss]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Ambiguous genitalia]], [[hypotension]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Ambiguous genitalia]], [[hypotension]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperkalemia]], increased [[17-alpha-hydroxyprogesterone|17 hydroxyprogestrone]], [[hyponatremia]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperkalemia]], increased [[17-alpha-hydroxyprogesterone|17 hydroxyprogestrone]], [[hyponatremia]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Salt wasting
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Salt wasting
 |-
-|align="center" style="background:#DCDCDC;"|[[Addison's disease]]
+| style="background:#DCDCDC;" align="center" |[[Addison's disease]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Skin [[hyperpigmentation]], [[fatigue]], salt craving, [[nausea and vomiting]], [[amenorrhea]], [[depression]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Skin [[hyperpigmentation]], [[fatigue]], salt craving, [[nausea and vomiting]], [[amenorrhea]], [[depression]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperpigmentation]], [[hypotension]], pubic and axillary hair loss
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperpigmentation]], [[hypotension]], pubic and axillary hair loss
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperkalemia]], decreased serum cortisol level
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperkalemia]], decreased serum cortisol level
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |Diagnosis by cosyntropin test
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |Diagnosis by cosyntropin test
 |-
-| rowspan="2" align="center" style="background:#DCDCDC;"|Tissue break down
+| style="background:#DCDCDC;" align="center" rowspan="2" |Tissue break down
-|align="center" style="background:#DCDCDC;"|[[Tumor lysis syndrome]]<ref name="pmid18509186">{{cite journal |vauthors=Coiffier B, Altman A, Pui CH, Younes A, Cairo MS |title=Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review |journal=J. Clin. Oncol. |volume=26 |issue=16 |pages=2767–78 |year=2008 |pmid=18509186 |doi=10.1200/JCO.2007.15.0177 |url=}}</ref>
+| style="background:#DCDCDC;" align="center" |[[Tumor lysis syndrome]]<ref name="pmid18509186">{{cite journal |vauthors=Coiffier B, Altman A, Pui CH, Younes A, Cairo MS |title=Guidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based review |journal=J. Clin. Oncol. |volume=26 |issue=16 |pages=2767–78 |year=2008 |pmid=18509186 |doi=10.1200/JCO.2007.15.0177 |url=}}</ref>
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Fever]], [[weight loss]], symptoms related to underlying malignancy
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Fever]], [[weight loss]], symptoms related to underlying malignancy
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Altered mental status]], [[lymphadenopathy]], [[muscle weakness]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Altered mental status]], [[lymphadenopathy]], [[muscle weakness]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperkalemia]], [[hyperphosphatemia]], [[hypocalcemia]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperkalemia]], [[hyperphosphatemia]], [[hypocalcemia]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |History of underlying malignancy
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |History of underlying malignancy
 |-
-|align="center" style="background:#DCDCDC;"|[[Rhabdomyolysis]]<ref name="pmid6282181">{{cite journal |vauthors=Knochel JP |title=Rhabdomyolysis and myoglobinuria |journal=Annu. Rev. Med. |volume=33 |issue= |pages=435–43 |year=1982 |pmid=6282181 |doi=10.1146/annurev.me.33.020182.002251 |url=}}</ref>
+| style="background:#DCDCDC;" align="center" |[[Rhabdomyolysis]]<ref name="pmid6282181">{{cite journal |vauthors=Knochel JP |title=Rhabdomyolysis and myoglobinuria |journal=Annu. Rev. Med. |volume=33 |issue= |pages=435–43 |year=1982 |pmid=6282181 |doi=10.1146/annurev.me.33.020182.002251 |url=}}</ref>
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Myalgia]], [[fatigue]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Myalgia]], [[fatigue]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Altered mental status]], [[hypotension]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Altered mental status]], [[hypotension]]
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperkalemia]], increased muscle enzymes (CK, aldolase)
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |[[Hyperkalemia]], increased muscle enzymes (CK, aldolase)
+| style="padding: 5px 5px; background: #F5F5F5;" align="center" |History of [[seizure]], [[drug overdose]], or [[trauma]]
-|style="padding: 5px 5px; background: #F5F5F5;" align="center" |History of [[seizure]], [[drug overdose]], or [[trauma]]
 |}
 |}

Hyperkalemia differential diagnosis: Difference between revisions

Revision as of 14:55, 16 July 2018

Overview

Differential Diagnosis

References

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