MENDOZA, DONNEMENDOZA, GRACIELLE

MENDOZA, TRISHAMINDANAO, MALVIN ACE

INFECTIOUS DISEASECONFERENCE

O.P.7 months, maleAugust 20, 2010157-2 M. Dela Fuente St. Sampaloc, ManilaRoman CatholicInformant: ParentsReliability: Good

DIARRHEA

HISTORY OF PRESENT ILLNESS

1 hr PTA 3 episodes of vomiting•amounting to 15mL/episode

- 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, (-) pruritusHEENT: (-) nasoaural discharge, (-) eye

discharge, (-) sore throatRespiratory: (-) dyspnea, (-) chest painCardiovascular: (-) palpitations, (-) cyanosis,

(-) easy fatigabilityGastrointestinal: SEE HPI

REVIEW OF SYSTEMS

Genitourinary: (-) dysuria (-) hematuriaMusculoskeletal: (-) weakness, (-)swellingHematopoietic: (-) easy bruisability, (-)

bleedingEndocrine: (-) polyuria, polydipsia,

polyphagiaNervous/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 AOGHep B screening and OGCT were not doneNo history of alcohol intake, smoking or

exposure to radiationNo illnesses noted during pregnancy

NEONATAL HISTORY

Born at 39-40 weeks AOGLive, singleton, delivered via NSDAPGAR score 8-9Birth weight = 2.7 kgBirth length – unrecalled1-day stay at the nurseryNo 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

AmountMacronutrients 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 12 8 10 170Cerelac 12 3 2,5 83SNACK        Milk 12 8 10 170DINNERMilk 12 8 10 170ACI 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 – PneumoniaJanuary 2011 - Diarrhea

FAMILY HISTORY

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

FAMILY PROFILE

Relation

AgeEducational Attainment

Occupation

Health

Mother 22High school

graduatenone Healthy

Father 27College

graduatePoliceman Healthy

PERSONAL, SOCIOECONIMIC AND ENVIRONMENTAL HISTORY

Apartment with both parentsWell-ventilated, well-litDrinking water is purifiedGarbage is not segregated but collected

everydayNo 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 36.9Wt 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 dermatosesPink palpebral conjunctiva, anicteric sclerae,

(+) sunken eyeballsNo 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 edemaNo genital lesions, no phimosisDRE: tight sphincteric tone, no tenderness,

no masses, brown fecal material on tactating finger, non-blood tinged

NEUROLOGIC EXAMINATION

Mental Status: alert, awakeCranial 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 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 volumeZinc sulfate 10mg/ml, 2ml once a day for 14

daysIVF 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

AcuteLess than 2 weeks

Chronic/PersistentMore than two weeks

Diarrhea: pathophysiology

OsmoticSecretoryIncreased/decreased intestinal motilityDecreased surface area

Diarrhea: pathophysiologyPRIMARY 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

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 DIARRHEASECRETORY 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

Infectious 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

InflammatoryUsually 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-inflammatoryEnterotoxin

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

ShigellaSalmonellaE coli: EPEC, EIEC, EAEC, ETEC, STECC jejuni

ETIOLOGYINCUBATION 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.

ETIOLOGYINCUBATION 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.

ETIOLOGYINCUBATION 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.

4–7 days 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.

Routine stool cultures

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 coliPathotype Epidemiology Type of

diarrheaMechanism 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

Watery 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

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 Normal to decreased Weak, thready, or impalpable

Breathing Normal Normal;fast Deep

Eyes Normal 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 Normal Prolonged Prolonged;minimal

Extremities Warm Cool Cold;mottled;cyanotic

Urine output Normal to decreased Decreased Minimal

CLINICAL IMPRESSION

ACUTE INFECTIOUS DIARRHEA WITH MODERATE SIGNS OF DEHYDRATION

CONFIRMATION OF WORKING DIAGNOSIS

STOOL EXAMINATION

Examine for mucus, blood and leukocytesFecal leukocytes are indicative of bacterial

invasion of colonic mucosaExamine for parasites causing diarrhea such

Giardia lamblia and E. histolyticaShouldd 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

1. Oral Rehydration Therapy2. Enteral feeding and diet selection3. Zinc supplementation4. 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 <6mosPrematurityChronic illnessFever >38C if <3mos or 39C if 3-36mosBloody diarrheaPersistent emesisPoor urine outputSunken eyesDepressed 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

10 mg/kg/d of TMP and 50 mg/kg/d of SMX bid × 5 d

Ciprofloxacin PO 20–30 mg/kg/d qid for 5–10 d

Salmonella No antibiotics for uncomplicated gastroenteritis in normal

GASTROENTERITISCommunity-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-compromisedstatus. Antibiotics generally notindicated otherwise.

Shigella TMP/SMX; Alt: Cefixime 5 days

GASTROENTERITIS

Community acquired

Yersinia TMP/SMX, aminoglycosides,cefotaxime, tetracycline (>8 yr).

Usually no antibiotic therapy isrecommended except withbacteremia, extraintestinalinfections, or immunocompromisedhosts.

Nosocomial Clostridium difficile

Metronidazole 7 days. Community organismsunlikely after 72 hr ofhospitalization.

N. PASHAPOUR, S. GOLMAHAMMADLOO PEDIATRICS DEPARTMENT, IMAM HOSPITAL

HEALTH DEPARTMENT, KOSAR HOSPITAL, URMIA, IRAN THE TURKISH JOURNAL OF PEDIATRICS 2006;

48: 115-118

EVALUATION OF YOGHURT EFFECT ON ACUTE DIARRHEA ON 6-24 MONTHS-

OLD HOSPITALIZED INFANTS

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

MalnutritionBloody stoolsNon-alimentary causes

RESULTS

Mean hospitalization days : 2.85 – 3.1Mean weight gain : 350 – 287.5Mean 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