Hypernatremia with hypokalemia

HOSP # MRN86510387 WARD Internal medicine
CONSULTANT Dr Jody Rusch   DOB/AGE 35 year female

Abnormal Result

Hypernatremia (sodium = 161 mmol/L)

Persistent Hypokalemia (potassium 1.9 mmol/L)

Presenting Complaint

Acute on chronic gastroenteritis

History

  • 35 year old female. Known HIV positive on ARV with weight loss. GIT symptoms. To exclude villous atrophy/parasitic infestation.
  • This is an HIV positive patient (CD4: 40 cells/uL; viral load: 54 869 copies/mL (4.74 log copies/ml))
  • The patient has had a CD4 < 150 since 2018.
  • HIV Viral load has never been suppressed <1000 copies / ml.
  • There are concerns of ARV compliance

Examination

Not available

Laboratory Investigations

Two days earlier:

Test Result
Sodium mmol/L 145
Potassium mmol/L 2.0 L
Chloride mmol/L 124 H
Urea mmol/L 7.9 H
Creatinine umol/L 246 H

Other Investigations

Histological examination requested after colonoscopy: Mild erythema of caecum. To exclude TB/CMV

Patient has undergone a colonoscopy as well as an enteroscopy and mild erythema of the caecum was seen.

The terminal ileum showed: intestinal metaplasia with preserved villous architecture. There is no evidence of active inflammation, ulceration or increased intraepithelial lymphocytes seen. There is no evidence of ova, viral inclusions, granulomas or parasites, and no evidence of dysplasia or malignancy present, hence no pathologic diagnosis.

The caecum biopsy, which was macroscopically erythematous, showed fragments of colonic mucosa with areas of crypt branching and focal gland associated neutrophils.

Final Diagnosis

Mild chronic active colitis.

Take Home Message

This patient, who has laboratory findings of AIDS, likely has a combination of aetiologies accounting for the deranged electrolytes. The acquired immune deficiency likely is complicated by repeated infections with accompanying inflammation of the colonic mucosa – this seems to have been ongoing for months already.

This may well likely have been causing dehydration which recently have caused acute kidney injury, with creatinine rising from a baseline of 86, three weeks prior, to ~250 umol/L.

Some simple bedside laboratory tests may be helpful in aetiological evaluation. In cases where diarrhea has persisted for more than two weeks, testing the stool for glucose and pH can be helpful in identifying those patients with severe villous atrophy. This can be done easily at the bedside with a urine dipstick if available. Glucose test tape, nitrazine paper, and Clinitest tablets also have been used. A stool glucose of greater than 2+ or a pH of less than 5.0 suggests substantial villous atrophy.



Hypernatremia

HOSP # WARD Red Cross Children’s Hospital ICU
CONSULTANT Dr. S
Prof. G		 DOB/AGE 14 day old Neonate

Abnormal Result

Sodium = 198 mmol/L (H) (136-145)

Presenting Complaint

1 day of poor feeding.  Child passing very hard/ dark brown stool for the preceding 10 days.

History

Birth weight @ term: 3.380kg.  Delivered vaginally after induction of labour because of spontaneous rupture of membranes at 40 weeks gestation. Discharged home without any problems after 1 day.

Examination

On arrival at district hospital: Temp: 38oC, Sats 96% on Nasal O2, Finger prick glucose: 10mmol/L, Capillary refill time: 6 seconds,

HR: 140bpm. 

Blood gas:

pH: 7.26,

BE -16.3,

pCO­2 3.2 kPa,

Na 190.

Weight: 2.2kg (birth weight: 3.380 kg, thus 35% weight loss)

Laboratory Investigations

Other Investigations

Urine organic acid analysis by GCMS demonstrates elevation of the liver markers 4-OH-phenyllactate and 4-OH-phenylpyruvate together with lactaturia. Succinylacetone, a marker for tyrosinaemia type 1 is absent. Moderate ketonuria with elevated dicarboxylic acids C6, C8, and C10 is also present, these changes suggest a lipolytic response to catabolic or fasting stress or hypoglycaemia together with underlying hepatic dysfunction with lactataemia but are non-specific for an IMD per se. 

Final Diagnosis

Patient was pure water depleted with a sodium concentration of 198 mmol/L.  The mother was not lactating adequately despite the infant sucking well, evidenced by the fact that when expressed breast milk was tried, there was too little milk for the baby to drink.  The nurses’ notes confirmed this finding.  This finding also confirms the failure to produce stool volume and the normal urine organic acid profile with evidence of starvation / fasting stress.

Take Home Messages

When considering a patient with high plasma sodium concentration it is
important to bear in mind:

  1. Hypernatremia does not necessarily indicate an excess of extracellular sodium.  Except in rare cases of salt overload most patient with hypernatremia have a deficiency of both water and sodium, with the water deficiency being proportionally higher than that of sodium.
  2. Patients become hypernatremic because the water lost from the body exceed the intake and there is negative fluid balance.  The amount of water which a person can drink generally exceeds by far the amount lost from the body in most pathological fluid-losing disorders, eg. Diarrhoea, sweating.  Patients thus become hypernatremia due to:
    1. Too old, young or sick to drink
    2. Obstruction of oesophagus
    3. Disorders of thirst centre
    4. No access to water                          

Ref: Walmsley – Cases in Chemical Pathology 4th
ed.

It is also important:

  1. To calculate the Osmolar gap( difference between calculated and measured osmolarity)
  2. U:P osmol (>1 = hypotonic fluid depletion, pure water loss or salt gain; ~1 = osmotic diuresis; <1 = diabetes insipidus ~the various causes of nephrogenic and neurogenic DI)