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Cholera Clinical Presentation

  • Author: Sajeev Handa, MBBCh, BAO, LRCSI, LRCPI; Chief Editor: Russell W Steele, MD  more...
 
Updated: Jun 27, 2016
 

History

After a 24- to 48-hour incubation period, symptoms begin with the sudden onset of painless watery diarrhea that may quickly become voluminous and is often followed by vomiting. The patient may experience accompanying abdominal cramps, probably from distention of loops of small bowel as a result of the large volume of intestinal secretions. Fever is typically absent.

However, most Vibrio cholerae infections are asymptomatic, and mild to moderate diarrhea due to V cholerae infection may not be clinically distinguishable from other causes of gastroenteritis. An estimated 5% of infected patients will develop cholera gravis, ie, severe watery diarrhea, vomiting, and dehydration.

Diarrhea

Profuse watery diarrhea is a hallmark of cholera. Cholera should be suspected when a patient older than 5 years develops severe dehydration from acute, severe, watery diarrhea (usually without vomiting) or in any patient older than 2 years who has acute watery diarrhea and is in an area where an outbreak of cholera has occurred.

Stool volume during cholera is more than that of any other infectious diarrhea. Patients with severe disease may have a stool volume of more than 250 mL/kg body weight in a 24-hour period. Because of the large volume of diarrhea, patients with cholera have frequent and often uncontrolled bowel movements.

The stool may contain fecal material early in the course of clinical illness. The characteristic cholera stool is an opaque white liquid that is not malodorous and often is described as having a “rice water” appearance (ie, in color and consistency, it resembles water that has been used to wash or cook rice).

Vomiting

Vomiting, although a prominent manifestation, may not always be present. Early in the course of the disease, vomiting is caused by decreased gastric and intestinal motility; later in the course of the disease it is more likely to result from acidemia.

Dehydration

If untreated, the diarrhea and vomiting lead to isotonic dehydration, which can lead to acute tubular necrosis and renal failure. In patients with severe disease, vascular collapse, shock, and death may ensue. Dehydration can develop with remarkable rapidity, within hours after the onset of symptoms. This contrasts with disease produced by infection from any other enteropathogen. Because the dehydration is isotonic, water loss is proportional between 3 body compartments, intracellular, intravascular, and interstitial.

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Physical Examination

Clinical signs of cholera parallel the level of volume contraction. The amount of fluid loss and the corresponding clinical signs of cholera are as follows:

  • 3-5% loss of normal body weight - Excessive thirst
  • 5-8% loss of normal body weight - Postural hypotension, tachycardia, weakness, fatigue, dry mucous membranes or dry mouth
  • >10% loss of normal body weight - Oliguria; glassy or sunken eyes; sunken fontanelles in infants; weak, thready, or absent pulse; wrinkled "washerwoman" skin; somnolence; coma
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Assessment for Dehydration

The World Health Organization has classified dehydration in patients with diarrhea into the following 3 categories, to facilitate treatment (see Table 1):

  • Severe
  • Some (previously termed moderate, in the WHO criteria)
  • None (previously termed mild, in the WHO criteria)

Children without clinically significant dehydration (< 5% loss of body weight) may have increased thirst without other signs of dehydration. In children with some (ie, moderate) dehydration, cardiac output and vascular resistance are normal, and changes in interstitial and intracellular volume are the primary manifestations of illness. Skin turgor is decreased, as manifested by prolonged skin tenting in response to a skin pinch (the most reliable sign of isotonic dehydration), and a normal pulse.

For the skin pinch, it is important to pinch longitudinally rather than horizontally and to maintain the pinch for a few seconds before releasing the skin. The skin pinch may be less useful in patients with marasmus (severe wasting), kwashiorkor (severe malnutrition with edema), or obesity.

In adults and children older than 5 years, other signs of severe dehydration include tachycardia, absent or barely palpable peripheral pulses, and hypotension.

Tachypnea and hypercapnia also are part of the clinical picture and are attributable to the metabolic acidosis that invariably is present in patients with cholera who are dehydrated.

Metabolic and systemic manifestations

After dehydration, hypoglycemia is the most common lethal complication of cholera in children. Hypoglycemia is a result of diminished food intake during the acute illness, exhaustion of glycogen stores, and defective gluconeogenesis secondary to insufficient stores of gluconeogenic substrates in fat and muscle.

Cholera causes bicarbonate loss in stools, accumulation of lactate because of diminished perfusion of peripheral tissues, and hyperphosphatemia. Acidemia results when respiratory compensation is unable to sustain a normal blood pH.

Hypokalemia results from potassium loss in the stool, with a mean potassium concentration of approximately 3.0 mmol/L. Because of the existing acidosis, however, children often have normal serum potassium concentrations when first observed, despite severe total body potassium depletion.

Hypokalemia develops only after the acidosis is corrected and intracellular hydrogen ions are exchanged for extracellular potassium. Hypokalemia is most severe in children with preexisting malnutrition who have diminished body stores of potassium and may be manifested as paralytic ileus.

Rehydration therapy with bicarbonate-containing fluids can also produce hypocalcemia by decreasing the proportion of serum calcium that is ionized. Chvostek and Trousseau signs are often present, and spontaneous tetanic contractions can occur.

Pediatric patients

In pediatric patients, the primary signs are similar to those in adults. However, children with severe cholera may present with signs that are rarely seen in adults. A child with cholera is usually very drowsy, and coma is not uncommon. In addition, pediatric patients may have convulsions that appear to be related, in part, to hypoglycemia because patients exhibit some response to intravenous dextrose. Another significant difference from the adult presentation is that children are often febrile.

Cholera sicca

Cholera sicca is an old term describing a rare, severe form of cholera that occurs in epidemic cholera. This form of cholera manifests as ileus and abdominal distention from massive outpouring of fluid and electrolytes into dilated intestinal loops. Mortality is high, with death resulting from toxemia before the onset of diarrhea and vomiting. The mortality in this condition is high. Because of the unusual presentation, failure to recognize the condition as a form of cholera is common.

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Table: Assessment for Dehydration

Table 1. Assessment of the Patient With Diarrhea for Dehydration (based on WHO classification) (Open Table in a new window)

Sensorium Eyes Thirst Skin Pinch Decision
Abnormally sleepy or lethargic Sunken Drinks poorly or not at all Goes back very slowly (>2 sec) If the patient has 2 or more of these signs, severe dehydration is present
Restless, irritable Sunken Drinks eagerly Goes back slowly (< 2 sec) If the patient has 2 or



more signs, some dehydration is present



Well, alert Normal Drinks normally, not



thirsty



Goes back quickly Patient has no dehydration
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Contributor Information and Disclosures
Author

Sajeev Handa, MBBCh, BAO, LRCSI, LRCPI Director, Division of Hospital Medicine, Department of Medicine, Rhode Island Hospital

Sajeev Handa, MBBCh, BAO, LRCSI, LRCPI is a member of the following medical societies: Society of Hospital Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

John W King, MD Professor of Medicine, Chief, Section of Infectious Diseases, Director, Viral Therapeutics Clinics for Hepatitis, Louisiana State University Health Sciences Center; Consultant in Infectious Diseases, Overton Brooks Veterans Affairs Medical Center

John W King, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Federation for Medical Research, Association of Subspecialty Professors, American Society for Microbiology, Infectious Diseases Society of America, Sigma Xi

Disclosure: Nothing to disclose.

Vidhu V Thaker, MBBCh, MD Attending Pediatrician, Haverstraw Pediatrics; Clinical Assistant Professor of Pediatrics, New York Medical College

Vidhu V Thaker, MBBCh, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Mark R Schleiss, MD Minnesota American Legion and Auxiliary Heart Research Foundation Chair of Pediatrics, Professor of Pediatrics, Division Director, Division of Infectious Diseases and Immunology, Department of Pediatrics, University of Minnesota Medical School

Mark R Schleiss, MD is a member of the following medical societies: American Pediatric Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Itzhak Brook, MD, MSc Professor, Department of Pediatrics, Georgetown University School of Medicine

Itzhak Brook, MD, MSc is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, Association of Military Surgeons of the US, Infectious Diseases Society of America, International Immunocompromised Host Society, International Society for Infectious Diseases, Medical Society of the District of Columbia, New York Academy of Sciences, Pediatric Infectious Diseases Society, Society for Experimental Biology and Medicine, Society for Pediatric Research, Southern Medical Association, Society for Ear, Nose and Throat Advances in Children, American Federation for Clinical Research, Surgical Infection Society, Armed Forces Infectious Diseases Society

Disclosure: Nothing to disclose.

References
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Electron microscopic image of Vibrio cholera.
Scanning electron microscope image of Vibrio cholerae bacteria, which infect the digestive system.
This scanning electron micrograph (SEM) depicts a number of Vibrio cholerae bacteria of the serogroup 01; magnified 22371x. Image courtesy of CDC/Janice Haney Carr.
This patient with cholera is drinking oral rehydration solution (ORS) in order to counteract the cholera-induced dehydration. Image courtesy of the CDC.
Table 1. Assessment of the Patient With Diarrhea for Dehydration (based on WHO classification)
Sensorium Eyes Thirst Skin Pinch Decision
Abnormally sleepy or lethargic Sunken Drinks poorly or not at all Goes back very slowly (>2 sec) If the patient has 2 or more of these signs, severe dehydration is present
Restless, irritable Sunken Drinks eagerly Goes back slowly (< 2 sec) If the patient has 2 or



more signs, some dehydration is present



Well, alert Normal Drinks normally, not



thirsty



Goes back quickly Patient has no dehydration
Table 2. Fluid Replacement for Dehydration
Severe dehydration Intravenous (IV) drips of Ringer Lactate or, if not available, normal saline and oral rehydration salts as outlined below
  • 100 mL/kg in 3-h period (in 6 h for children < 1 y)
  • Start rapidly (30 mL/kg within 30 min, then slow down)
  • Total amount for first 24 h: 200 L/kg
Some dehydration Oral rehydration salts (amount in first 4 h)
  • Infants < 4 mo (< 5 kg): 200–400 mL
  • Infants 4–11 mo (5–7.9 kg): 400–600 mL
  • Children 1–2 y (8–10.9 kg): 600–800 mL
  • Children 2–4 y (11–15.9 kg): 800–1200 mL
  • Children 5–14 y (16–29.9 kg): 1200–2200 mL
  • Patients >14 y (≥30 kg): 2200–4000 mL
No dehydration Oral rehydration salts
  • Children < 2 y: 50–100 mL, up to 500 mL/day
  • Children 2–9 y: 100–200 mL, up to 1000 mL/day
  • Patients >9 y: As much as wanted, up to 2000 mL/day
Table 3. Approximate Amount of Oral Rehydration Solution to Administer in the First 4 Hours
Age < 4 mo 4-11 mo 12-23 mo 2-4 y 5-14 y ≥15 y
Weight < 5 kg 5-7.9 kg 8-10.9 kg 11-15.9 kg 16-29.9 kg ≥30 kg
ORS solution in mL 200-400 400-600 600-800 800-1200 1200-2200 2200-4000
Table 4. Estimate of Oral Rehydration Solution Packets to Be Administered at Home
Age Amount of Solution After Each Loose Stool ORS Packets Needed
< 24 mo 50-100 mL Enough for 500 mL/d
2-9 y 100-200 mL Enough for 1000 mL/d
≥10 y As much as is wanted Enough for 200 mL/d
Table 5. Oral Replacement Solution for Maintenance of Hydration
Age Amount of Solution After Each Loose Stool
< 24 mo 100 mL
2-9 y 200 mL
≥10 y As much as is wanted
Table 6. Antimicrobial Therapy Used in the Treatment of Cholera*
Antibiotic Single Dose (PO) Multiple Dose (PO)
Doxycycline 7 mg/kg; not to exceed 300 mg/dose 2 mg/kg bid on day 1; then 2 mg/kg qd on days 2 and 3; not to exceed 100 mg/dose
Tetracycline 25 mg/kg; not to exceed 1 g/dose 40 mg/kg/d divided qid for 3 d; not to exceed 2 g/d
Furazolidone 7 mg/kg; not to exceed 300 mg/dose 5 mg/kg/d divided qid for 3 d; not to exceed 400 mg/d
Trimethoprim and sulfamethoxazole Not evaluated < 2 months: Contraindicated



≥2 months: 5-10 mg/kg/d (based on trimethoprim component) divided bid for 3 d; not to exceed 320 mg/d trimethoprim and 1.6 g/d of sulfamethoxazole



Ciprofloxacin§ 30 mg/kg; not to exceed 1 g/dose 30 mg/kg/d divided q12h for 3 d; not to exceed 2 g/d
Ampicillin Not evaluated 50 mg/kg/d divided qid for 3 d; not to exceed 2 g/d
Erythromycin Not evaluated 40 mg/kg/d erythromycin base divided tid for 3 d; not to exceed 1 g/d
* Antimicrobial therapy is an adjunct to fluid therapy of cholera and is not an essential component. However, it reduces diarrhea volume and duration by approximately 50%. The choice of antibiotics is determined by the susceptibility patterns of the local strains of V cholerae O1 or O139.



Tetracycline and doxycycline can discolor permanent teeth of children younger than 8 years. However, the risk is small when these drugs are used for short courses of therapy, especially if used in a single dose.



Single-dose therapy of these drugs has not been evaluated systematically in children, and recommendations are extrapolated from experience in adults.



§ Fluoroquinolones (eg, ciprofloxacin) are not approved in the United States for use in persons younger than 18 years. When given in high doses to juvenile animals, they cause arthropathy. Clinical experience indicates that this risk is very small in children when used for short courses of therapy.



Table 7. WHO Guidelines for Cholera Management
Steps in the treatment of a patient with suspected cholera are as follows:
1. Assess for dehydration (see Table 1)
2. Rehydrate the patient and monitor frequently, then reassess hydration status
3. Maintain hydration; replace ongoing fluid losses until diarrhea stops
4. Administer an oral antibiotic to the patient with severe dehydration
5. Feed the patient
More detailed guidelines for the treatment of cholera are as follows:
  • Evaluate the degree of dehydration upon arrival
  • Rehydrate the patient in 2 phases; these include rehydration (for 2-4 h) and maintenance (until diarrhea abates)
  • Register output and intake volumes on predesigned charts and periodically review these data
  • Use the intravenous route only (1) during the rehydration phase for severely dehydrated patients for whom an infusion rate of 50-100 mL/kg/h is advised, (2) for moderately dehydrated patients who do not tolerate the oral route, and (3) during the maintenance phase in patients considered high stool purgers (ie, >10 mL/kg/h)
  • During the maintenance phase, use oral rehydration solution at a rate of 800-1000 mL/h; match ongoing losses with ORS administration
  • Discharge patients to the treatment center if oral tolerance is greater than or equal to 1000 mL/h, urine volume is greater than or equal to 40 mL/h, and stool volume is less than or equal to 400 mL/h.
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