INFECTIOUS DISEASE CONFERENCE Mendoza, Donne mendoza, gracielle Mendoza, trisha Mindanao, malvin ace

DIARRHEA O.P. 7 months, male August 20, 2010 157-2 M. Dela Fuente St. Sampaloc, Manila Roman Catholic Informant: Parents Reliability: Good DIARRHEA

HISTORY OF PRESENT ILLNESS 3 episodes of vomiting amounting to 15mL/episode 1 hr PTA - 4 episodes of loose, mucoid, yellowish stool, altogether amounting to 200mL - Noted to be weak-looking, w/ cold clammy skin 30 min PTA ADMISSION

REVIEW OF SYSTEMS Cutaneous: (-) rashes, (-) pruritus HEENT: (-) nasoaural discharge, (-) eye discharge, (-) sore throat Respiratory: (-) dyspnea, (-) chest pain Cardiovascular: (-) palpitations, (-) cyanosis, (-) easy fatigability Gastrointestinal: SEE HPI

REVIEW OF SYSTEMS Genitourinary: (-) dysuria (-) hematuria Musculoskeletal: (-) weakness, (-)swelling Hematopoietic: (-) easy bruisability, (-) bleeding Endocrine: (-) polyuria, polydipsia, polyphagia Nervous/Behavior: (-) headache, (-) seizures, (-)tremors, (-) loss of consciousness

GESTATIONAL HISTORY Born to a 22 y/o G1P0 mother with a common law 27 y/o policeman partner Regular prenatal check-up since 5 mo AOG Hep B screening and OGCT were not done No history of alcohol intake, smoking or exposure to radiation No illnesses noted during pregnancy

NEONATAL HISTORY Born at 39-40 weeks AOG Live, singleton, delivered via NSD APGAR score 8-9 Birth weight = 2.7 kg Birth length – unrecalled 1-day stay at the nursery No complications noted during delivery

FEEDING HISTORY Breastfed exclusively for 1 month More than 8 times per day or everytime child cries Shifted to milk formula Mother claimed she was not producing enough milk Bottlefed since 2 months until present 2-5 months: S26 – 1:2 dilution, 4 oz per feeding, 6x /day 6 months to present: Bonamil – 1:2 dilution, 8 oz per feeding, 4-5x/day Complementary feeding started at 6 months Cerelac and pureed food

24 – HR FOOD RECALL Amount Macronutrients Total CHO (4 cal/g) CHON (4 cal/g) Fats (9 cal/g) Kilocalories BREAKFAST   Milk 1:2 8 oz 12 8 10 170 SNACK LUNCH Milk Cerelac 3 2,5 83 DINNER ACI 763 RENI 720 % 106%

DEVELOPMENT/BEHAVIORAL HISOTRY Gross motor With good head control, can crawl, rolls over, sits with support Fine motor Transfers object from 1 hand to another Language Imitates speech sounds Personal Social Laughs and plays with examiner

IMMUNIZATIONS HEALTH CENTER BCG – 1 dose Hep B – 1 dose DPT – 3 doses OPV – 3 doses Hib – 1 dose

PAST MEDICAL HISTORY October 2010 – Pneumonia January 2011 - Diarrhea

FAMILY HISTORY (+) HPN – maternal grandmother (-) DM, goiter, asthma, cancer, TB

Educational Attainment FAMILY PROFILE Relation Age Educational Attainment Occupation Health Mother 22 High school graduate none Healthy Father 27 College graduate Policeman

PERSONAL, SOCIOECONIMIC AND ENVIRONMENTAL HISTORY Apartment with both parents Well-ventilated, well-lit Drinking water is purified Garbage is not segregated but collected everyday No nearby factories, no pets

PHYSICAL EXAMINATION Alert, awake, weak-looking, with moderate signs of dehydration, drinks eagerly, not in cardiorespiratory distress VS: CR 160 RR 40 T 36.9 Wt 6 kg. (z= 0) Lt. 73 cm (z= 0) AC: 43 cm BMI 11 (z= below -3) wt. for Ht. (z= below -3)

PHYSICAL EXAMINATION Warm, dry skin, no active dermatoses Pink palpebral conjunctiva, anicteric sclerae, (+) sunken eyeballs No tragal tenderness, non-hyperemic EAC, (+) retained cerumen, AU, intact tympanic membrane, no aural discharge AU Midline septum, turbinates not congested, no nasal discharge

PHYSICAL EXAMINATION Dry buccal mucosa, no oral lesions, to non-hyperemic posterior pharyngeal wall, tonsils not enlarged Supple neck, no palpable cervical lymphadenopathies or anterior neck masses Symmetrical chest expansion, no retractions, clear breath sounds Adynamic precordium, apex beat 4th LICS MCL, no heaves, thrills, murmurs

PHYSICAL EXAMINATION Globular abdomen, NABS, soft, non- tender, no mass palpated Pulses full and equal, no cyanosis, no edema No genital lesions, no phimosis DRE: tight sphincteric tone, no tenderness, no masses, brown fecal material on tactating finger, non-blood tinged

NEUROLOGIC EXAMINATION Mental Status: alert, awake Cranial Nerves are intact: intact EOM; no ptosis; no jaw deviation; smiles, open and close his eyes, no facial asymmetry; midline uvula, no tongue atrophy, no fasciculations, no deviation No Babinski, no nuchal rigidity

SALIENT FEATURES POSITIVE NEGATIVE 7 mo/male Diarrhea – mucoid stools Vomiting Weak-looking, with cold clammy skin Past medical history of diarrhea (+) sunken eyeballs dry buccal mucosa drinks eagerly NEGATIVE (-) fever (-) abdominal pain

ADMITTING IMPRESSION DIARRHEA

APPROACH TO DIAGNOSIS Look for a symptom, sign, or laboratory finding pointing to a group of diseases

COURSE IN THE WARDS

DAY 1 CBC with platelet count and fecalysis were done. CBC showed normal results, while fecalysis showed pus cells of over 100/hpf, RBC of (+), and macrophage of (+), and stool culture was then requested. ORS 75 to replace losses volume per volume Zinc sulfate 10mg/ml, 2ml once a day for 14 days IVF started at D5 0.3% NaCl 100%.

DAY 2 & DAY 3 Ciprofloxacin 16.6 mg/kg/day given for 3 days. IVF given was D5 0.3 NaCl at 100%.  DAY 4 & DAY 5 Discharged improved and stable

Diarrhea: definition Increased total daily stool output, usually associated with increased stool water content Stool output more than 10g/kg/24hr or more than the adult limit of 200 g/24hr Results from altered intestinal water and electrolyte transport GIT of infant handles approx 285 ml/kg/24hr of fluid (intake plus intestinal secretion) with a stool output of 5-10g/kg/24hr

Diarrhea: chronicity Acute Less than 2 weeks Chronic/Persistent More than two weeks

Diarrhea: pathophysiology Osmotic Secretory Increased/decreased intestinal motility Decreased surface area

Diarrhea: pathophysiology PRIMARY MECHANISM DEFECT STOOL EXAMINATION EXAMPLES COMMENT Secretory Decreased absorption, increased secretion, electrolyte transport Watery, normal osmolality; osmoles = 2 × (Na+ + K+) Cholera, toxigenic E. coli; carcinoid, VIP, neuroblastoma, congenital chloride diarrhea, Clostridium difficile, cryptosporidiosis (AIDS) Persists during fasting; bile salt malabsorption may also increase intestinal water secretion; no stool leukocytes Osmotic Maldigestion, transport defects ingestion of unabsorbable Watery, acidic, and reducing substances; increased osmolality; osmoles >2 × (Na+ + K+) Lactase deficiency, glucose-galactose malabsorption, lactulose, laxative abuse Stops with fasting; increased breath hydrogen with carbohydrate malabsorption; no stool leukocytes

Decreased transit time PRIMARY MECHANISM DEFECT STOOL EXAMINATION EXAMPLES COMMENT Increased motility Decreased transit time Loose to normal-appearing stool, stimulated by gastrocolic reflex Irritable bowel syndrome, thyrotoxicosis, postvagotomy dumping syndrome Infection may also contribute to increased motility Decreased motility Defect in neuromuscular unit(s) Stasis (bacterial overgrowth) Loose to normal appearing stool Pseudoobstruction, blind loop Possible bacterial overgrowth Decreased surface area (osmotic, motility) Decreased functional capacity Watery Short bowel syndrome, celiac disease, rotavirus enteritis May require elemental diet plus parenteral alimentation Mucosal invasion Inflammation, decreased colonic reabsorption, increased motility Blood and increased WBCs in stool Salmonella, Shigella, infection; amebiasis; Yersinia, Campylobacter infections Dysentery evident in blood, mucus, and WBCs

Diarrhea: pathophysiology   OSMOTIC DIARRHEA SECRETORY DIARRHEA Volume of stool <200 mL/24 hr >200 mL/24 hr Response to fasting Diarrhea stops Diarrhea continues Stool Na+ <70 mEq/L >70 mEq/L Reducing substances[*] Positive Negative Stool pH <5 >6 fasting stops persists example Lactose intolerance Cholera, ETEC

Acute diarrhea Non-infectious Protein intolerance Intussusception Bacteria B. cereus C. jejuni C. perfringens E. Coli (STEC, EIEC) Salmonella spp Shigella spp S. aureus V. cholerae V. parahaemolyticus V. vulnificus Virus Norovirus Calicivirus Rotavirus Astrovirus Adenovirus Parvovirus Protozoa G. Lamblia Non-infectious Protein intolerance Intussusception Meckel’s diverticulum Food hypersensitivity Food-induced enterocolitis Ciguater fish poisoning Mushroom poisoning Nitrite poisoning Organophosphates Puffer fish (tetrodotoxin) Scombroid (histamine) Shellfish poisoning Heavy metals Sb, As, Cd, Cu, Hg, Zn, Th

Acute infectious diarrhea Inflammatory Usually bacteria that directly invades the intestines or produce cytotoxins with consequent fluid, protein and cells that enter the intestinal lumen Presents as bloody mucoid stool Fecalysis: + fecal leukocytes Non-inflammatory Enterotoxin production by some bacteria (cholera), destruction of villous cells by viruses (rotavirus), adherence by parasites (G lamblia), and adherence and or translocation by bacteria

Acute infectious inflammatory diarrhea Shigella Salmonella E coli: EPEC, EIEC, EAEC, ETEC, STEC C jejuni

ETIOLOGY INCUBATION PERIOD SIGNS AND SYMPTOMS DURATION OF ILLNESS ASSOCIATED FOODS LABORATORY TESTING TREATMENT Campylobacter jejuni 2–5 days Diarrhea, cramps, fever, and vomiting; diarrhea may be bloody. 2–10 days Raw and undercooked poultry, unpasturized milk, contaminated water Routine stool culture; Campylobacter requires special media and incubation at 42°C to grow. Supportive care. For severe cases, antibiotics such as erythromycin and quinolones may be indicated early in the diarrheal disease. Guillain-Barré syndrome can be a sequela. Enterotoxigenic E. coli (ETEC) 1–3 days Watery diarrhea, abdominal cramps, some vomiting 3 to >7 days Water or food contaminated with human feces Stool culture. ETEC requires special laboratory techniques for identification. If suspected, must request specific testing. Supportive care. Antibiotics are rarely needed except in severe cases. Recommended antibiotics include TMP-SMX and quinolones.

ETIOLOGY INCUBATION PERIOD SIGNS AND SYMPTOMS DURATION OF ILLNESS ASSOCIATED FOODS LABORATORY TESTING TREATMENT Enterohemorrhagic E. coli (EHEC) including E. coli O157 : H7 and other Shiga toxin–producing E. coli (STEC) 1–8 days Severe diarrhea that is often bloody, abdominal pain and vomiting. Usually, little or no fever is present. More common in children <4 yr old. 5–10 days Undercooked beef especially hamburger, unpasteurized milk and juice, raw fruits and vegetables (e.g., sprouts), salami (rarely), and contaminated water Stool culture; E. coli O157 : H7 requires special media to grow. If E. coli O157 : H7 is suspected, specific testing must be requested. Shiga toxin testing may be done using commercial kits; positive isolates should be forwarded to public health laboratories for confirmation and serotyping. Supportive care, monitor renal function, hemoglobin, and platelets closely. E. coli O157 : H7 infection is also associated with hemolytic uremic syndrome (HUS), which can cause lifelong complications. Studies indicate that antibiotics may promote the development of HUS.

ETIOLOGY INCUBATION PERIOD SIGNS AND SYMPTOMS DURATION OF ILLNESS ASSOCIATED FOODS LABORATORY TESTING TREATMENT Salmonella spp. 1–3 days Diarrhea, fever, abdominal cramps, vomiting. S. typhi and S. paratyphi produce typhoid with insidious onset characterized by fever, headache, constipation, malaise, chills, and myalgia; diarrhea is uncommon, and vomiting is not usually severe. 4–7 days Contaminated eggs, poultry, unpasteurized milk or juice, cheese, contaminated raw fruits and vegetables (alfalfa sprouts, melons). S. typhi epidemics are often related to fecal contamination of water supplies or street-vended foods. Routine stool cultures Supportive care. Other than for S. typhi and S. paratyphi, antibiotics are not indicated unless there is extra-intestinal spread, or the risk of extra-intestinal spread, of the infection. Consider ampicillin, gentamicin, TMP-SMX, or quinolones if indicated. A vaccine exists for S. typhi. Shigella spp. 24–48 hr Abdominal cramps, fever, and diarrhea. Stools may contain blood and mucus. Food or water contaminated with human fecal material. Usually person-to-person spread, fecal-oral transmission. Ready-to-eat foods touched by infected food workers, e.g., raw vegetables, salads, sandwiches. Supportive care. TMP-SMX recommended in the U. S. if organism is susceptible; nalidixic acid or other quinolones may be indicated if organism is resistant, especially in developing countries.

Escherichia coli Pathotype Epidemiology Type of diarrhea Mechanism of pathogenesis STEC Hemorhagic colitis and HUS in all ages and postdiarrheal thrombotic thrombocytopenic purpura in adults Bloody or non-bloody Large bowel adherence and effacement (AE), shiga toxin production EPEC Acute and chronic endemic and epidemic in infants Watery Small bowel AE ETEC Infantile diarrhea in resource-limited countries and traveler’s diarrhea in all ages Small bowel AE, heat stable/ heat labile enterotoxin production EIEC Diarrhea with fever in all ages Bloody or non-bloody; dysentery Adherence, mucosal invasion and inflammation of large bowel EAEC Acute and chronic diarrhea in all ages Watery, occasionally bloody Small and large bowel adherence, enterotoxin and cytotoxin production

DEHYDRATION Mental status Thirst Heart rate Quality of pulses SYMPTOM MINIMAL OR NO DEHYDRATION (<3% LOSS OF BODY WEIGHT) MILD TO MODERATE DEHYDRATION (3–9% LOSS OF BODY WEIGHT) SEVERE DEHYDRATION (>9% LOSS OF BODY WEIGHT) Mental status Well;alert Normal, fatigued or restless, irritable Apathetic, lethargic, unconscious Thirst Drinks normally; might refuse liquids Thirsty;eager to drink Drinks poorly; unable to drink Heart rate Normal Normal to increased Tachycardia, with bradycardia in most severe cases Quality of pulses Normal to decreased Weak, thready, or impalpable Breathing Normal;fast Deep Eyes Slightly sunken Deeply sunken Tears Present Decreased Absent Mouth and tongue Moist Dry Parched Skinfold Instant recoil Recoil in <2 sec Recoil in >2 sec Capillary refill Prolonged Prolonged;minimal Extremities Warm Cool Cold;mottled;cyanotic Urine output Minimal

CLINICAL IMPRESSION ACUTE INFECTIOUS DIARRHEA WITH MODERATE SIGNS OF DEHYDRATION

CONFIRMATION OF WORKING DIAGNOSIS

STOOL EXAMINATION Examine for mucus, blood and leukocytes Fecal leukocytes are indicative of bacterial invasion of colonic mucosa Examine for parasites causing diarrhea such Giardia lamblia and E. histolytica Shouldd be obtained as early in the course of disease as possible from children with bloody diarrhea

STOOL CULTURE Should be obtained as early in the course of disease as possible from children with bloody diarrhea in whom stool microscopy indicates fecal leukocytes

TREATMENT

Principles of Management Oral Rehydration Therapy Enteral feeding and diet selection Zinc supplementation Antibiotic therapy

Oral Rehydration Therapy Children especially infants are more susceptible than adults to dehydration because of the greater basal fluid and electrolyte requirements. Dehydration must be evaluated rapidly and corrected 4-6hrs according to the degree of dehydration.

Oral Rehydration Therapy Those in shock or unable to tolerate fluids, require initial intravenous rehydration but oral rehydration is the preferred mode of replacing ongoing losses.

Risks associated with severe dehydration that necessitate IV resuscitation Age <6mos Prematurity Chronic illness Fever >38C if <3mos or 39C if 3-36mos Bloody diarrhea Persistent emesis Poor urine output Sunken eyes Depressed level of consciousness

Oral Rehydration Therapy Decarbonated soda beverages, fruit juices are not suitable for rehydration as they have inappropriately high osmolalities and low sodium concentrations ORS should be given to infants and children slowly, especially if they have emesis It can be given by a dropper, teaspoon or syringe. The volume is increased as tolerated.

Enteral Feeding and Diet Selection Continued enteral feeding in diarrhea aids in recovery and age appropriate diet after rehydration is the norm. Once rehydration is complete, food should be reintroduced while oral rehydration can be continued to replace ongoing losses from emesis or stools.

Enteral feeding and Diet Selection Breast feeding should be resumed as soon as possible Foods with complex carbohydrates, yogurt, fruits and vegetables are also tolerated Fatty foods or foods high in simple sugars should be avoided.

Zinc supplementation Zinc leads to reduced duration and sseverity of diarrhea and could potentially prevent 300,000 deaths. WHO and UNICEF recommend that all children with acute diarrhea should recive oral zinc for 10-14 days during and after diarrhea 10mg/day for infants <6mos 20mg/day >6mos

Antibiotic Therapy Timely antibiotic therapy may reduce the duration and severity of diarrhea and prevent complications. While these agents are important to use in specific cases, their widespread and indiscriminate use leads to development of resistance.

ORGANISM DRUG OF CHOICE DOSE AND DURATION OF TREATMENT Shigella (severe dysentery and EIEC dysentery) Ciprofloxacin, ampicillin, ceftriaxone, or trimthoprim-sulfamethoxazole Ceftriaxone IV, IM 50–100 mg/kg/d qd, bid × 7 d Most strains are resistant to many antibiotics Ciprofloxacin PO 20–30 mg/kg/d bid × 7–10 d 10 mg/kg/d of TMP and 50 mg/kg/d of SMX bid × 5 d Ampicillin PO, IV 50–100 mg/kg/d qid × 7 d EPEC, ETEC, EIEC TMP-SMX or ciprofloxacin Ciprofloxacin PO 20–30 mg/kg/d qid for 5–10 d Salmonella No antibiotics for uncomplicated gastroenteritis in normal

GASTROENTERITIS Community-acquired Viruses, E. coli Antibiotic therapy strongly discouraged because of increased risk of HUS occurring in patients with E. coli 0157:H7 treated with antibiotics Primary treatment: fluid and electrolyte replacement Salmonella Cefotaxime or Ceftriaxone 10-14 days for infants <6 mo, toxicity or immuno-compromised status. Antibiotics generally not indicated otherwise. Shigella TMP/SMX; Alt: Cefixime 5 days

GASTROENTERITIS Community acquired Yersinia TMP/SMX, aminoglycosides, cefotaxime, tetracycline (>8 yr). Usually no antibiotic therapy is recommended except with bacteremia, extraintestinal infections, or immunocompromised hosts. Nosocomial Clostridium difficile Metronidazole 7 days. Community organisms unlikely after 72 hr of hospitalization.

N. Pashapour, S. Golmahammadloo Pediatrics Department, Imam Hospital EVALUATION OF YOGHURT EFFECT ON ACUTE DIARRHEA ON 6-24 MONTHS-OLD HOSPITALIZED INFANTS N. Pashapour, S. Golmahammadloo Pediatrics Department, Imam Hospital Health Department, Kosar Hospital, Urmia, Iran The Turkish Journal of Pediatrics 2006; 48: 115-118

OBJECTIVES To determine the efficacy of local factory pasteurized yoghurt consumption in acute nonbloody and mucoid diarrhea on hospitalized 6-24 months infants as compared with that of routine treatment

SUBJECTS 6 to 24 months of age children with non-bloody and mucoid diarrhea with less than four days duration hospitalizing in Urmia; Imam Hospital 2 GROUPS (20 EACH) Control group: routine hospital treatment only Case group: received at least 15 ml/kg/day of pasteurized cow milk yogurt orally plus routine hospital treatment Weight gain, period of hospitalization and reduction of diarrhea were compared

EXCLUSION Malnutrition Bloody stools Non-alimentary causes

RESULTS  reduction of diarrhea episodes Mean hospitalization days : 2.85 – 3.1 Mean weight gain : 350 – 287.5 Mean reduction of diarrhea episodes : 4.35 – 3.95 Significant difference (P<0.50)  reduction of diarrhea episodes

CONCLUSION Use of local pasteurized yoghurt in the treatment of acute diarrhea had positive effects As a probiotic, it can promote recovery from diarrhea in children, mainly non-bloody Universal use of yoghurt is recommended in acute non-bloody diarrhea