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Electrolytes Abnormalities means the abnormal function of body fluid that plays a vital role in maintaining homeostasis within the body. They help to regulate heart and neurological function, fluid balance, oxygen delivery, acid-base balance and much more. Electrolyte imbalances can develop by the following mechanisms: excessive ingestion; diminished elimination of an electrolyte; diminished ingestion or excessive elimination of an electrolyte. The most serious electrolyte disturbances involve abnormalities in the levels of sodium, potassium or calcium. Other electrolyte imbalances are less common and often occur in conjunction with major electrolyte changes. Chronic laxative abuse or severe diarrhea or vomiting (gastroenteritis) can lead to electrolyte disturbances along with dehydration. People suffering from bulimia or anorexia nervosa are at especially high risk for an electrolyte imbalance.

Electrolyte Abnormalities

Routine laboratory studies are common in the intensive care unit; abnormalities are even more common. Typically these studies include a chemistry panel (Chem 10). The differential diagnoses of the most frequent and clinically relevant electrolyte abnormalities are detailed below.

Differential Diagnosis and Evaluation of Hyponatremia

Differential Diagnosis and Evaluation of Hypernatremia

Differential Diagnosis and Evaluation of Hypokalemia

Differential Diagnosis of Hyperkalemia

Differential Diagnosis of Hypo and Hypercalcemia

Differential Diagnosis of Hypo and Hypermagnesemia

Differential Diagnosis of Hypo and Hyperphosphatemia

Hyponatremia

62M with a history of hepatitis C cirrhosis complicated by hepatocellular carcinoma s/p radiofrequency ablation presenting after referral from hepatology clinic for hyponatremia. One week ago, the patient developed abdominal distension and shortness of breath that resolved after large-volume paracentesis and was started on furosemide 40mg p.o. daily and aldactone 100mg p.o. daily.

After initiating diuretics, the patient noted worsening lower extremity edema, and increased thirst/fluid intake.

He reports two days of fatigue and intermittent confusion supported by family members who reported slowed speech. He otherwise denies abdominal pain, distension, nausea/vomiting, diarrhea/constipation, chest pain or shortness of breath. In the ED, the patient received 1L NS bolus.

PMH:

Hepatitis C cirrhosis c/b HCC s/p RFA
Rheumatoid arthritis, well-controlled without medications

PSH:

None

FH:

Non-contributory.

SHx:

Lives with partner, denies current or prior t/e/d abuse
HepC contracted from blood transfusions

Meds:

Furosemide 40mg p.o. daily
Spironolactone 100mg p.o. daily
Rifaximin 550mg p.o. b.i.d.

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Allergies

NKDA

Physical Exam

VS:	T	98.2	HR	80	RR	14	BP	95/70	O2	98% RA
Vent:	PRVC, VT 320, RR 35, PEEP 6, FiO2 95%
Gen:	Elderly female in no acute distress, alert and answering questions appropriately.
HEENT:	NC/AT, PERRL, EOMI, no scleral icterus, MMM.
CV:	RRR, normal S1/S2, no murmurs. JVP 8cm.
Lungs:	Faint basilar crackles on bilateral lung bases.
Abd:	Normoactive bowel sounds, non-distended, non-tender, without rebound/guarding.
Ext:	2+ pitting edema in lower extremities to knees bilaterally. 2+ peripheral pulses, warm and well perfused.
Neuro:	AAOx3. CN II-XII intact. No asterixis. Normal gait. Normal FTN/RAM.

Labs/Studies

BMP (admission): 112/5.6/88/22/28/1.1/97
BMP (+10h): 118/5.4/93/23/26/1.0/133
sOsm: 264
Urine: Na <20, K 26, Osm 453
BNP: 40
AST/ALT/AP/TB/Alb: 74/57/91/2.4/2.2

Assessment/Plan

62M hx HepC cirrhosis, newly decompensated with e/o decompensation (new-onset ascites) and hyponatremia.
# hyponatremia: Sodium 114, likely chronic, patient currently asymptomatic without concerning findings on neurological exam. Clinical findings suggestive of hypervolemic hyponatremia 2/2 decompensated cirrhosis resulting in decreased effective arterial blood volume and volume retention. However, the recent initiation of diuretics, mild AKI and early response to isotonic fluids in the ED suggests possible hypovolemic component.

1L fluid restriction
q.4.h. sodium check, goal increase of 8mEq per 24h
hold diuretics

# hyperkalemia: Potassium 5.6, asymptomatic, AKI vs. medication-induced (aldactone). Continue monitoring.
# AKI: Elevated creatinine 1.1 from baseline 0.7. Likely pre-renal given recent initiation of diuretics. Consider hepatorenal syndrome given decompensated cirrhosis. Follow-up repeat creatinine after 1L NS bolus in ED.
# hepatitis C: decompensated with new-onset ascites. No e/o encephalopathy, continue home rifaximin.

Physiology of Hyponatremia

Differential Diagnosis of Hyponatremia

Evaluation of Hyponatremia

Identification of onset (acute vs. chronic)
Presence of symptoms (HA, nausea, confusion, seizures)
Assessment of volume status (edema, JVD, skin turgor, postural BP)
Medical history (cardiac, liver, renal disease), drug history

Hyperglycemic Crises

Blurred vision, numbness

HPI:

56 year-old male with a history of DM, questionable HTN presenting with blurred vision, numbness of fingertips/toes for 2wks. Associated symptoms include dry mouth, polydipsia/polyuria. He states that these symptoms coincide with elevated measurements of blood glucose at home (>500). He ran out of his diabetes medication (metformin) 8mo ago but states his BG was typically between 100-200 with diet/exercise until 2wks ago. He reports recent dietary indiscretions on a trip to Las Vegas.

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He denies fevers/chills, CP/SOB, cough, abdominal pain, N/V, or dysuria.

PMH:

DM II
HTN

PSH:

None

FH:

Several maternal family members with DM.

SHx:

No tobacco/drug use
5-6 alcoholic drinks/wk

Meds:

Metformin 500mg p.o. b.i.d.

Allergies:

NKDA

Physical Exam

VS:	T 37.8 HR 60 RR 14 BP 165/90 O2 99% RA
Gen:	Well-appearing, no acute distress, obese
HEENT:	PERRL, EOMI, optic discs sharp b/l, no abnormalities visualized
CV:	RRR, normal S1/S2, no M/R/G, no additional heart sounds
Lungs:	CTAB, no wheezes/crackles
Abd:	+BS, soft, NT/ND, no rebound/guarding
Ext:	Warm, well-perfused, 2+ pulses, no clubbing/cyanosis/edema
Neuro:	AAOx3, CN II-XII intact

Labs/Studies

BMP: 135/3.8/102/24/18/1.1/378
CBC: 7.4/14.1/42.0/403
UA: + glucose, – ketones

Assessment/Plan

56M, hx DM with poor medication adherence presenting with vision changes and stocking/glove paresthesias for 2wks after reported dietary indiscretion found to be hyperglycemic. DKA/HHS unlikely given stable vital signs, normal metabolic panel with exception of isolated hyperglycemia (slight hyponatremia likely related to osmotic effect of elevated serum glucose). Also, no evidence of concerning precipitates for hyperglycemic crisis (no CP/SOB, no F/C, no cough, no abdominal pain, no change in mental status). Patient was discharged home with education on importance of medication adherence, refill of metformin, and follow-up with primary care physician for further management of DM and possible hypertension.

Evaluation of hyperglycemic crises in patients with diabetes

Key signs/symptoms of HHS/DKA

Both: Polyuria, polydipsia, weight loss, hypovolemia (dry MM, skin turgor, tachycardia, hypotension)
DKA: Short course (<24h), N/V, diffuse abdominal pain, Kussmaul respirations
HHS: Longer course (days/weeks), altered mental status (lethargy, coma, seizure)

Admission Laboratory Data of Patients with HHS vs. DKA

	DKA	HHS
Glucose (mg/dl)	616	930
pH	7.12	7.30
3-β-hydroxybutyrate (mmol/l)	9.1	1.0
Serum osmolality	323	380
Delta gap (AG-12)	17	11
Na (mEq/l)	134	149
K (mEq/l)	4.5	3.9
Bicarbonate (mEq/l)	9	18

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Delirium, ID

A 70 year-old female with a PMH of HTN, DM, hyperlipidemia and stage I breast cancer s/p lumpectomy with sentinel LN biopsy several years ago presented for elective surgery complicated by post-operative bleeding. She is now 4 days post-op and was found to be confused, somnolent and occasionally agitated.

HPI:

The patient could not be interviewed.

PE:

VS: Stable and within normal limits
General: unremarkable except for crackles in bilateral lung bases
MSE: only arouses to sternal rub and becomes agitated, moving all four extremities spontaneously and symmetrically.
Reflexes: corneal and gag reflexes present, suppresses eye movements with head turn, deep tendon reflexes 3+ throughout UE/LE bilaterally.

Assessment

70 year-old woman with a history of HTN, DM, hyperlipidemia and breast cancer presents with worsening confusion, somnolence and occasional agitation four days after surgery. The combination of significantly altered consciousness and absence of focal neurological findings, all in the setting of a complicated surgical course suggest delirium.