Case Study One: A severe case of relapsing cholera



|TM5559: Clinical Tropical Paediatrics |

|Case Study One: A severe case of relapsing cholera |

|Samantha Leggett: SN 12494652 |

| |

|19/01/2011 |

Case Study One

Samantha Leggett

A relapsing case of severe Cholera

Demographic Information

The patient is a young boy who will be identified as W, of approximately eight years of age. His ethnicity is Bamu and he lives in Emeti, a small village on the Bamu River in the Middle Fly district of Western Province, Papua New Guinea (PNG). W lives with his mother, father and two younger siblings and the family are members of the Church of the Latter Day Saints.

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Past History

According to his father W had received treatment for severe malaria earlier this year and had suffered from ‘sotwind’ [1]since he was a small boy. W appeared fairly under nourished in contrast to his parents and siblings who, unusually compared to the majority of other villagers, appeared relatively well nourished and healthy despite a total absence of health care in the immediate region and a diet largely consisting of sago[2]. The child’s health record was not available in order for an assessment to be made regarding growth, development and immunisation status.

Background

In the mid afternoon of 29/11/10 during an emergency intervention in response to a cholera outbreak, W was carried into our rudimentary Cholera Treatment Unit (CTU)[3] in Sogere village by his father. W had an overnight history of five watery stools with no vomiting or abdominal pain. The family had had to wait for high tide and had then journeyed a number of hours down river in their dugout canoe to the CTU to seek help. W had had little to drink since the onset of the diarrhoea.

Examination and course of admission

On assessment W appeared moderately dehydrated with a palpable radial pulse, sunken eyes, some irritability, a skin pinch return of around two seconds and slightly dry mucous membranes. He was alert and engaged well and drank eagerly when given Oral Rehydration Salts (ORS). At this point I diagnosed him as having cholera with moderate dehydration. Unfortunately W had a large vomit after his first cup of ORS and then refused to drink any more. As a precaution, instead of being assessed on an outpatient basis, W was admitted to the CTU for closer observation. When presented with the choice of having a needle put in his arm or drinking more ORS W chose the oral fluid option. Throughout the afternoon and early evening he drank a litre of ORS with some diarrhoea but no more vomiting. He also managed a small meal of banana and sago at about 8pm. Shortly after this W decided that he wanted to join his mother and siblings outside and took himself off while his father was going to the toilet.

When his father returned I gave him a 600ml bottle of ORS and instructions to ask W to drink at least a third of it before bed and then drink more if he had diarrhoea in the night. I also asked W’s father to bring him back for assessment before he himself went to sleep or before this if W’s diarrhoea increased in frequency or severity.

The two returned at around midnight and W was in good spirits having had only one more episode of watery diarrhoea and no more vomits. He’d managed to drink around 100mls more of ORS. I agreed that he could spend the night with his family but re-iterated to his father that he must return if W became unwell again.

At 5.30am on 30/11/10 W’s father carried him back into the CTU saying that he had started having profuse diarrhoea again over the previous few hours and had not had any more ORS to drink. Upon assessment W was severely shocked with a non-palpable radial pulse and a thready and rapid brachial pulse, very sunken eyes, a skin pinch return of >4 seconds, and was moribund and freezing cold.

A second and blind attempt at intravenous (IV) cannulation secured tenuous access and I sat with W and his father holding the line in for over an hour while I administered two volumes of resuscitation fluids as rapidly as the IV access would allow. With an estimated weight of 20kg W was given 2 x 600mls of IV Ringer Lactate with 20mls IV Dextrose 50% added to the first 600mls. His family had little in the way of warm clothing or bedding so we covered him with his father’s sweatshirt and some black plastic sheeting. His condition had not improved after the first volume of fluid but after the second he became more responsive and his radial pulse was once again palpable. His IV fluids were then adjusted for rehydration and maintenance and as he became more responsive I encouraged him to begin drinking ORS again. During the resuscitation period W had two more watery stool of a moderate volume. The outcome of this case was a positive one with W being discharged from the CTU two days later eating and drinking well and with no more diarrhoea for the preceding twenty four hours.

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1. W post-resuscitation fluid

Cholera Overview

Cholera is an acute diarrhoeal disease resulting from the colonization of the small intestine by the bacteria Vibrio Cholerae of which there are numerous serogroups. Of these, only V. cholerae 01 and V. cholerae 0139 are associated with the epidemiological characteristics and clinical picture of cholera. If V. cholerae breaches the gastric acid defence the vibrios multiply rapidly in the alkaline environment of the small intestine and disease is caused by the exotoxins that they release. Subunit B of the toxin adheres to the intestinal mucosa which permits subunit A entry into the cells. Subunit A then activates cyclic adenosine monophosphate (cAMP) which results in the loss of water, bicarbonate and electrolytes from the cells. The exotoxins effectively act as pumps, moving water from cells in the blood and tissues, into the intestinal lumen [1, 2, 3, 4].

The disease is clinically characterised by an acute onset of profuse painless watery diarrhoea flecked with mucous and epithelial cells (‘rice water stools’) and is often associated with vomiting large amounts of fluid. It can result in rapid dehydration and electrolyte depletion which without prompt recognition and treatment can result in acidosis, cardiovascular collapse and death. In its extreme form cholera is one of the most rapidly fatal illnesses known today [4].

With this in mind, in most cases of cholera (75-80%) the infection is asymptomatic or only causes mild diarrhoea although in both situations it is still possible to transmit the disease. Cholera is a self limiting illness and the diarrhoea usually ceases within a week if the patient survives. Deaths from cholera are largely due to dehydration but can also result from hypoglycaemia and renal failure (although this is commonly as a result of protracted dehydration arising from insufficient fluid replacement) [5]. Without treatment >50% of severe cases will die; with prompt and adequate treatment the Case Fatality Rate (CFR) should be ................
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