A rare case of hypokalaemia and hypophosphataemia secondary to geophagia
- 1 Department of Internal Medicine, Livingstone Hospital, Port Elizabeth, South Africa
- 2 Department of Medicine, Walter Sisulu University, Port Elizabeth, South Africa
- 3 Department of Medicine, Division Nephrology and Hypertension, University of Cape Town, Port Elizabeth, South Africa
- Correspondence to Dr Robert Freercks; robert.freercks@uct.ac.za
Abstract
We report a case of severe hypokalaemia and moderate hypophosphataemia from clay ingestion. A 60-year-old woman presented with flaccid paralysis. Investigations revealed a serum potassium level of 1.8 mmol/L, phosphate level of 0.56 mmol/L and creatine kinase level of 30 747 IU/L. She had marked proximal and distal muscle weakness due to severe hypokalaemia and concurrent hypophosphataemia, which likely contributed to the onset of rhabdomyolysis. The patient subsequently admitted to significant pica, most likely secondary to an associated iron deficiency. We conclude that the ingested clay acted as a potassium and phosphate binder. Although we did not investigate the content of the clay in this case, it has been reported that clay can bind potassium in vitro and is rich in minerals such as aluminium that could play a role in the binding of phosphate, although the exact mechanism remains unclear. The patient recovered fully and outpatient follow-up at 6 months and again at 40 months confirmed no electrolyte abnormality, myopathy nor any further geophagia.
Background
The deliberate consumption of earth, soil or clay, known as geophagia, is the most common form of pica.1 2 In particular, geophagia is most commonly observed during pregnancy or as a feature of iron deficiency anaemia.3 Ingested clay causes increased intestinal loss of potassium as the clay binds to potassium ions.4 Potassium regulates skeletal muscle arterial flow and vascular tone and severe depletion may cause local ischaemia and muscular damage.5 Hypophosphataemia can also cause rhabdomyolysis through depletion of ATP and the consequent inability of muscle cells to maintain membrane integrity.6 We report here a case of flaccid paralysis and rhabdomyolysis as a consequence of hypokalaemia and hypophosphataemia.
Case presentation
A 60-year-old female patient presented to our service with flaccid paralysis. She reported a 1-week history of progressive muscle weakness, rendering her unable to walk. She also reported abdominal pain, constipation, loss of appetite and weight loss of approximately 10 kg in 1 year. She reported no gynaecological symptoms.
Her medical history included a smoking history of 20 pack-year and uncontrolled hypertension for which she was not on any treatment. She did not abuse alcohol, non-steroidal anti-inflammatory drugs nor illicit substances and was on no chronic medication. Family and travel history were unremarkable.
Examination revealed an elderly woman with sarcopaenia and a body mass index of less than 18 kg/m2. She appeared pale. Her blood pressure on admission was 193/93 mm Hg. The rest of her vitals were normal.
Her abdomen was diffusely tender on deep palpation, but no signs of peritonism or organomegaly were noted. Bowel sounds were present. Rectal examination revealed compact, grey stools. Higher mental functions were normal and there was no cranial nerve fallout. She had generalised proximal and distal muscle weakness with inability to lift her head off the pillow. All of her limbs were hypotonic with diminished but present reflexes. Cardiovascular, respiratory and rheumatological examination was normal.
Investigations
Initial biochemistry identified severe hypokalaemia and moderate hypophosphataemia in the presence of normal renal function. Full blood count revealed a microcytic anaemia with thrombocytosis, most likely due to associated iron deficiency. The arterial blood gas revealed a mild metabolic alkalosis in keeping with severe hypokalaemia. There was evidence of rhabdomyolysis, with an elevated creatine kinase level and elevated transaminases with reversed aspartate aminotransferase to alanine transaminase ratio. The urine phosphate:creatinine ratio was elevated and the fractional excretion of phosphate was 53% (table 1).
Biochemical investigations on admission and follow-up
| Blood parameters | On admission | 24 hours after treatment started | 6-month follow-up | 40-month follow-up | Normal range |
|---|---|---|---|---|---|
| Sodium (mmol/L) | 145 | 136–145 | |||
| Potassium (mmol/L) | 1.8 | 2.7 | 4.5 | 4.3 | 3.5–5.1 |
| Urea (mmol/L) | 2.2 | 2.8 | 2.1–7.1 | ||
| Creatinine (μmol/L) | 47 | 49 | 49–90 | ||
| Creatine kinase (U/L) | 30 747 | 28 063 | 20–180 | ||
| Alanine transaminase (U/L) | 228 | 7–35 | |||
| Aspartate aminotransferase (U/L) | 906 | 13–35 | |||
| Alkaline phosphatase (U/L) | 67 | 42–98 | |||
| Gamma-glutamyl transferase (U/L) | 28 | <40 | |||
| White cell count (×109/L) | 10.4 | 3.90–12.60 | |||
| Haemoglobin (g/dL) | 7.9 | 13.4 | 12–15 | ||
| Mean corpuscular volume (fL) | 77.4 | 112 | 78.9–98.5 | ||
| Platelet count (×109/L) | 512 | 283 | 186–454 | ||
| Calcium (mmol/L) | 2.02 | 2.30 | 2.34 | 2.20–2.55 | |
| Magnesium (mmol/L) | 0.89 | 0.89 | 0.63–1.05 | ||
| Phosphate (mmol/L) | 0.56 | 1.08 | 1.35 | 1.12 | 0.78–1.42 |
| Parathyroid hormone (pmol/L) | 2.4 | 1.3 - 9.3 | |||
| Iron (umol/L) | 2.7 | 12.5 | 9.0–30.4 | ||
| Ferritin (g/L) | 17 | 335 | 11–307 | ||
| Transferrin (g/L) | 2.06 | 2.58 | 1.90–3.75 | ||
| Saturation (%) | 5 | 19 | 15–50 | ||
| Aldosterone (pmol/L) | <27 | 160 | 49–643 | ||
| Renin (Miu/L) | 1.4 | 52.6 | 2.0–36.4 | ||
| Urine phosphate (mmol/L) | 14 | 2.39 | 14.74 | 0.74–1.4 | |
| Urine creatinine (mmol/L) | 2.2 | 2.7 | 4.7 | 6–13 | |
| Urine potassium (mmol/L) | 7.3 | 19.9 | 0–10 | ||
| Urine phosphate:creatinine ratio (mmol/mmol) | 6.7 | 0.88 | 1.21 | 0.38–3.95 | |
| Urine potassium:creatinine ratio (mmol/mmol) | 3.3 | 4.23 | In the presence of hypokalaemia, a ratio >1.5 is suggestive of renal losses | ||
| Urine chloride (mmol/L) | 97 | 58 | 20–40 |
Treatment
The patient was moved to a high care unit, where she received intravenous potassium and phosphate replacement. She was also treated with phosphate-based enemas to disimpact the bowel. The patient showed remarkable improvement over 3 days and was able to lift her head off the pillow and mobilise. The electrolytes normalised and she was discharged home after 7 days.
Outcome and follow-up
The patient’s muscle weakness improved dramatically after replacement of phosphate and potassium via central venous catheter infusions in hospital. She recovered well and was discharged home after 7 days. At her 6-month follow-up, she had no residual electrolyte abnormalities and her muscle power proximally and distally had returned to normal. Furthermore, there was no further geophagia. She was still noted to be markedly sarcopaenic and work up for her weight loss was ongoing. At clinical review 40 months after the initial admission, she was still well and denied any loss of appetite or concerning symptoms. Her weight was identical to her 6 months follow-up and she denied further geophagia. The work-up for malignancy and tuberculosis was negative and repeat abdominal radiograph showed no evidence of clay ingestion. Her biochemistry remained within normal limits and the arterial blood gas was normal. The fractional excretion of phosphate at follow-up was normal.
Discussion
The patient reported here presented with flaccid paralysis due to severe hypokalaemia and hypophosphataemia from clay ingestion. Geophagia is the deliberate consumption of earth, clay and soil and is one of the most common forms of pica. We believe she had pica associated with an iron deficiency anaemia. Although geophagia itself has been documented as a contributing cause of iron deficiency anaemia, other more common causes for iron deficiency should be excluded as the consequence of geophagia.7 8 She did not report further clay ingestion in her subsequent clinic follow-up visits, confirming that her pica symptoms improved as her iron deficiency was treated.
The patient’s profound hypokalaemia was attributed to the long-term intestinal binding of the clay to potassium ions. Other causes of hypokalaemia were not found. While the urine potassium:creatinine ratio is usually <1.5 mmol/mmol in the presence of extrarenal potassium losses, it was 3.3 mmol/mmol in our patient, suggesting a concomitant degree of renal potassium loss. However, the absolute urine potassium was low at 7.3 mmol/L and was measured once the patient was already receiving high-dose intravenous potassium.9 Furthermore, her sarcopaenia would skew this result further in reducing 24-hour urinary creatinine excretion, thereby overestimating renal losses when using a reference range that assumes an average 24-hour creatinine excretion of 10 mmol/24 hours.10–12 Therefore, we postulate that her potassium deficiency was still consistent with extrarenal loss. This is further supported by the normalising of her serum electrolytes off supplementation at 6-month follow-up and after cessation of geophagia. However, it is possible that a degree of transient tubular dysfunction due to hypokalaemic nephropathy contributed to some renal losses of potassium, especially in view of her phosphaturia.
We noted moderate hypophosphataemia despite the concomitant rhabdomyolysis and observed an increase in the urinary creatinine:phosphate ratio. The raised urinary fractional excretion of phosphate is indicative of inappropriate urinary phosphate loss. Increased urinary phosphate loss secondary to hypokalaemia has previously been described in case reports and in a study in rats, hypokalaemia has been shown to be associated with inhibition of sodium phosphate cotransport.13 14 The hypophosphataemia could also be attributed to the functioning of the clay as a phosphate binder (similarly to the binding of clay to the potassium ions) and thus decreasing the absorption of phosphate. Clay is rich in various minerals, such as aluminium.15 Aluminium is used in patients with chronic kidney disease to lower serum phosphate levels and thus could have also played a role in the mechanism of phosphate binding.16 However, this mechanism does not explain the high urinary excretion of phosphate and it is likely that a combination of the above two mechanisms caused the low serum phosphate. There was no other evidence for an underlying generalised tubular defect in that she had no glycosuria, no acidosis and no persistent abnormalities in serum electrolytes after extended follow-up.
The skeletal muscle weakness and severe rhabdomyolysis was likely a complication of severe hypokalaemia and hypophosphataemia. Hypokalaemia causes significant muscle weakness at serum potassium concentrations below 2.5 mEq/L. The pattern of weakness usually begins in the lower extremities, progresses to the trunk and upper extremities and can worsen to the point of paralysis. In addition to causing muscle weakness, severe potassium depletion (serum potassium less than 2.5 mEq/L) can lead to rhabdomyolysis and myoglobinuria.17–20 Profound hypokalaemia can diminish blood flow to muscles during exertion, leading to ischaemic rhabdomyolysis.20 When severe hypokalaemia is combined with hypophosphataemia, myocyte injury and rhabdomyolysis are further exacerbated due to ATP depletion, mitochondrial dysfunction, oxygen free-radical production5 and the inability of muscle cells to maintain membrane integrity.5 6 21
In conclusion, we report here a rare case of severe hypokalaemia and hypophosphataemia secondary to geophagia, associated with paralysis. To the best of our knowledge, only one other case report describes hypokalaemia and hypophosphataemia associated with geophagia.22 A careful history remains key and clinicians should maintain a high index of suspicion for pica and its attendant complications, especially in the presence of an iron deficiency anaemia and muscle weakness.
Learning points
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Clinicians should have a high index of suspicion for pica especially in the context of iron deficiency anaemia.
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Geophagia is a common form of pica and clinicians should include direct questions around the condition when taking the patients history.
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Hypokalaemia and hypophosphataemia can cause severe weakness and rhabdomyolysis.
Acknowledgments
The authors wish to thank Professor Razeen Davids for his kind review of the manuscript.
Footnotes
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Contributors All three authors were involved in the management and investigations of the case presented. CS was involved with manuscript write up, literature review and informed consent. JOO was involved in the initial management of the patient and conceptualising of the manuscript. RF was involved in the manuscript review as the senior author and critical appraisal.
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Funding The authors wish to thank the Kidneys, Infectious Diseases and Critical Care (KICC) Public Benefit Organisation for funding of publication costs for this manuscript.
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Competing interests None declared.
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Provenance and peer review Not commissioned; externally peer reviewed.
- © BMJ Publishing Group Limited 2021. No commercial re-use. See rights and permissions. Published by BMJ.
References
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