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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