Hematemesis in children-Beyond Infancy
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Transcript of Hematemesis in children-Beyond Infancy
Hematemesis in Children- Beyond Infancy
Dr. Divya NairDNB PediatricsMahavir Hospital.
Gastrointestinal (GI) bleeding in children is a fairly common problem
In the pediatric ICU population, 6-20% have upper GI bleeds. The incidence of lower GI bleeding has not been well established
10-20% of referrals to pediatric gastroenterologists
Upper gastrointestinal (UGI) bleeding originating from esophagus, stomach or duodenum-proximal to the ligament of Treitz (aka duodenojejunal ligament)
Commonly presents with hematemesis (vomiting of blood or coffee ground-like material) and/or melena (black, tarry stools)
Etiology:A) Gastrointestinal causes
B) Systemic causes
C) Genetic causes
D) Spurious causes
A) Gastrointestinal causes:
1) Esophagitis:
GERD
Hiatus Hernia
Infection: e.g. Candida,
Aspergillus, CMV, HSV
Medications: e.g. tetracycline,
aspirin, NSAIDs, potassium chloride
“ erosive esophagitis"
2) Esophageal Rupture
Mallory-Weiss Syndrome (located at LES)
3) Gastritis: More common than ulcers Medications (e.g. NSAIDs, aspirin) Infections (e.g., Helicobacter pylori, CMV,
herpes) Crohn’s disease
4) Gastric Erosions:
Trauma, burn, shock or sepsis
This is usually superficial and occurs mainly in the
fundus of the stomach
5) Peptic Ulcer Disease
6) Zollinger-Ellison syndrome Gastrinoma Results in multiple
diffuse GI/ small bowel
ulcerations
Ulcer with red spot
Bleeding Ulcer
7)Portal hypertension: Esophageal varices Gastric varices Hypertensive gastropathy
Cirrhosis due to congenital
hepatitis, hepatic fibrosis,
cystic fibrosis
8) Extra-hepatic portal vein
obstruction
Esophageal varices
9) Vascular malformations:
Hemangiomas
Aorto-esophageal/-enteric fistulas
Dieulafoy ulcer (superficial defect of gastric mucosa which overlies an ectatic submucosal a.)
Watermelon stomach (gastric antral vascular ectasia)
Vasculitis eg: ITP
10) Tumors:
Polyps
Lipomas, leiomyoma
Adenocarcinoma
Lymphoma
Metastatic tumors,
Kaposi’s sarcoma, Barrett’s esophagus
Kasabach-Merritt synd (Hemangioma thrombocytopenia
syndrome)
11) Traumatic: Prolapsing gastropathy
Foreign body ingestion
Direct abdominal trauma
12) Iatrogenic- throat/nose Sx,
traumatic NG
13) Miscellaneous:
Hemobilia
Hemosuccus pancreaticus
Menetries’ Disease
Eosinophilic enteropathy
Munchausen by proxy syndrome
Barrett’s ulcer secondary to GERD
B) Systemic Causes:1) Coagulopathy (congenital/acquired): Hemophilia,
vWD
2) Sepsis, scarlet fever, malaria, leptospirosis
3) Burns, Sepsis ( Curling’s ulcer),
Raised ICT, Head injury, Encephalitis ( Cushing’s ulcer)
4) HUS, HSP
5) Malignancy- Leukemia
6) Poisonings- chemical, caustic
7) Drugs-aspirin, NSAIDS, anti-coagulants
8) Food (milk protein) allergy/ hypersensitivity
9) Idiopathic
NSAID induced Ulcers
C) Genetic conditions:Turner syndrome
Ehlers Danlos syndrome
( cutis hyperelastica)
Pseudoxanthoma elasticum
Klippel Trenaunay syndrome
Osler-Rendu-Weber syndrome
(hereditary hemorrhagic telangectesia)
Blue rubber bleb naevus syndrome
Hermansky-Pudlak syndrome
D) Spurious causes:
I) Hematememis: Bleeding from nose (epistaxis),
mouth, pharynx,
hemoptysis
II) Malena: Iron preparation, Bismuth, Lead,
spinach, beets,
blueberries
Grading of UGI BleedsMILD: presents as nausea, vomiting, abdominal discomfort & small
quantity of hematemesis/ malena
MODERATE: significant blood loss, tachycardia, cold sweat, hypo-
tension.
No ongoing blood loss; recovers with blood transfusion
SEVERE: more striking features of shock present, Hb falls to 8gm%
or less.
Requires multiple blood transfusions d/t ongoing blood loss
Takes longer time to recover; very high mortality unless treated
properly.
Diagnosis:
History Quantity, frequency, type of blood
(bright red vs coffee ground)
Nausea, vomiting, recurrent abdominal pain s/o PUD
Dysphagia/ odynophagia, chest pain/burning,
hematochezia, melena, bruising, bleeding, repeated retching f/b vomiting of
blood
Weight loss, early satiety s/o malignancy
Psychiatric symptoms
Drug ingestion
Bleeding sites- skin, mucosa, GUT, joints
Recurrent epistaxis
H/O Jaundice, stool color
Severe and diffuse upper GI ulcerations with chronic diarrhea usually : Zollinger Ellison syndrome or gastrinoma
Birth history: lines placed (umbilical lines can result in clotting of portal vein)
Past history: History of liver disease,
history of pancreatitis, GI surgeries
H/O Bleeding disorders in family
Medications: NSAID use, aspirin use
Diet history: Formula intolerance, food
allergies
Physical examination:Vitals:- Heart rate, respiratory rate, BP, capillary refill, orthostatic changes
Pallor
During examination of the head, ears, eyes, nose, and throat, look for causes such as:
epistaxis, nasal polyps, and oropharyngeal erosions from caustics and other ingestions
Signs of Chronic Liver Disease: Jaundice, Clubbing, leukonychia, palmar erythema, spider nevi, gynecomastia, etc.
Vascular malformations: hemangiomas, telangiectasias or purpura over skin
Peutz- Jeghers syndrome: pigmented lips, palms, soles
Pseudoxanthoma elasticum: “Plucked chicken appearance” of skin
Per Abdomen:Tenderness, Hyperactive bowel sounds
Caput medusa with ascites, shrunken liver and
splenomegaly s/o Cirrhosis with Portal Hypertension
Extra-hepatic PHT will have splenomegaly without hepatomegaly
Spleen may contract following
a massive bleed and may
not be palpable (Smith
Howard Syndrome)
Work up:
CBP, PCV, RBS
Coagulation studies
LFT to r/o cirrhosis
RFT
Type and cross-match of several units of blood
Oesophago-gastro-duodenoscopy : If active bleeding, most sensitive and specific for diagnosis and provides therapeutic options
Ultrasound with Doppler to assess liver disease and portal hypertension
In episodic or obscure bleeding : nuclear medicine radionucleotide studies, arteriography, and wireless video capsule endoscopy are used to assist in identifying the site of blood loss
Special tests:
Serum gastrin levels ( Zollinger Ellison syndrome)
Peroxide based tests: Gastroccult for upper GI bleed
Gastroccult : only test designed specifically for detecting gastric occult blood and determining gastric pH
It includes a convenient pH comparison chart for the Clinically relevant range which is important in monitoring antacid prophylaxis
Certain ingestions such as red meat, iron, and peroxidase-containing vegetables (eg: turnips, horseradish, broccoli, cauliflower, and cantaloupe), can give false-positive results
Imaging:Barium contrast studies- barium swallows, upper GI series, small bowel
follow-throughs, or barium enemas : for non emergency bleeds, to
point to foreign bodies, ulcers, IBD, or polyps
Endoscopy:
Patients with severe upper GI bleeding should receive endoscopy within the first 12 hours of the hemorrhagic episode if they are sufficiently stable, because early endoscopy improves the diagnostic index
The site of upper GI bleeding can be identified in 90% of cases when endoscopy is performed within 24 hours
This modality is also beneficial in predicting the likelihood of continued bleeding
The Forress classification divides endoscopic findings into the following 3 categories:
I - Active hemorrhage (Ia = bright-red bleeding,
Ib = slow bleeding)
II - Recent hemorrhage (IIa = non-bleeding visible vessel,
IIb = adherent clot on base of lesion,
IIc = flat pigmented spot)
III - No evidence of bleeding
Arteriography :
used to localize lesions when endoscopy has failed
or when the patient cannot cooperate
Detects vascular lesions in esophagus, stomach,
hepatic aneurysms & pseudo-
cysts of pancreas
The modality can be helpful
for bleeding that is distal to
the ligament of Treitz
Management:Initial approach
to ensure patient stability,
to establish adequate oxygen delivery,
to place intravenous access,
to initiate fluid and blood resuscitation,
to correct any underlying coagulopathies
Children at low risk for recurrent or life-threatening hemorrhage may be suitable for early hospital discharge or even outpatient care
All patients with hemodynamic instability/ active bleeding should be admitted in ICU for resusitation and close observation
ICU Requirements:
Pediatric Intensivist, Pediatric Surgeon, Pediatric Gastroenterologist,
Invasive monitors, Ventilators, Attached blood bank, Trained nursing
staff
i) Big bore canula (IV/ IO)
Hydration-NS/ RL
SOS Transfusion
ii) ICU care, invasive monitoring in unstable patients
Cardiorespiratory monitor, intake- output chart,
catheterization to monitor UO
CVP monitoring helps to guide replacement therapy
Inj Vit K 5mg to be given in case of hepatocellular
failure, cholestatic jaundice.
iii) NG aspiration:
Every ½ to 1 hourly for next 24 hours
If significant blood loss estimated; as it ascertains fresh
blood, decreases aspiration risk and aids in visualization via
endoscope
Gastric lavage with normal saline
Iced saline does not stop bleeding and may even cause
central hypothermia in a small child.
iv) Endoscopic therapy including:
1. Sclerotherapy (EST): The best Em/El procedure
Acts by producing intimitis thrombosis fibrosis of
the vessels
Sclerosants: Ethanolamine oleate 5%
Sodium morrhuate 5%
Sodium tetradecylsulphate 1.5%
Cx: Esophageal ulceration, stricture, Broncho-
esophageal fistula, thoracic duct damage,
recurrance of varices, transient bacteremia
2. Variceal banding: became popular b’cos of Cx of
EST, but it is difficult in children
Elastic band occludes the varix and it is necrosed &
sloughed off in 5-10 days
3. Heater probe and bipolar coagulation for ulcers
v) Sengstaken Blakemore tube/ Minnesota tube:
Mechanical Tamponade by balloons which
compresses esophageal & gastric varices
Has 3 lumens- for gastric and esophageal balloons
& for aspiration of gastric contents
Effectively controls acute bleeding, but assosiated
with significant no. of Cx
and rebleeding when tube
is removed
vi) Transjugular Intrahepatic Porto-systemic Shunt (TIPSS):
Percutaneous technique that creates a shunt in the
liver between the portal & hepatic veins
Indications: Refractory variceal h’age
Refractory ascites
Hepatorenal syndrome
CI: Polycystic liver disease, Right Heart Failure,
Systemic Infections, PV thrombosis, Biliary obstruction, severe hepatic
encephalopathy
Cx: Acute thrombosis or Delayed stenosis of shunt, Hepatic
Encephalopathy
vii) Selective embolization
viii) Laparoscopy/ Laparotomy
Surgical repair rarely indicated:
1) Pt with EHPHT is from a remote area without facilities for EST/
blood transfusions
2) Pt continues to bleed from ectopic varices/ persistent esophageal
varices, despite EST
3) Hypersplenism
Surgeries done for PHT: Decompressive Shunts
Devascularization
Liver Transplantation
Pharmacotherapy:ix) Antacids:
H2 blockers, Proton pump inhibitors: used as common causes of GI bleed
are gastritis and peptic ulcer disease.
Aluminium & Magnesium hydroxide
x) Children known to have cirrhosis should receive Antibiotics,
prefrebly before endoscopy, as bacterial infections are present
in upto 20% of these patients
Treat infections including triple therapy (antibiotics and proton pump
inhibitor) for H. pylori
Remove allergen in case of allergy
xi) Hormones/ hormone analogues (reduces splanchnic blood
flow for variceal bleeding by vasoconstriction) :
1) Somatostatin- polypeptide,
inhibits release of vasodialatory GI peptides
eg glucagon, VIP & sustance P
Dose: 250microgm IV bolus f/b 250microgm/hr
infusion
Disadvn: very short ½ life
2) Octreotide-synthetic analogue of somatostatin,
much longer ½ life & hence can be given as bolus or
infusion
Dose: 1microgm/kg IV infusion over 30min f/b
0.5microgm/kg/hour
Disadvn: Exorbitant cost
Nausea, flatulence, malabsorbtion (supresses GI
motility & secretion)
Bowel ischemia in high doses
3) Vasopressin-non peptide, derived from posterior pituitary gland
Splanchnic vasoconstriction, constricts lower
esophageal sphincter
Dose: 0.33unit/kg over 20min f/b IV infusion of
0.33units/kg/hour
S/E: CVS-myocardial ischemia/infarction, VF (can
be decreased by combining it with Nitroglycerine)
Cerebral H’age, Respiratory arrest,
Bowel ischemia & necrosis
4) Terlipressin (Triglycyl-lysine vasopressin)
Synthetic analogue of vasopressin
Long duration of action & less cardiac S/E
Dose: 2mg IV q6h until bleeding stops f/b 1mg q6h for next
24hrs
5) Miscellaneous Drugs:
Clonidine (α2 agonist)
Ketanserine & Ritanserine (5HT2 receptor antagonists)
Molsidomine (venodialator)
Prophylaxis Against Bleed From Variceal
Hemorrhage and Ulceration
Primary prophylaxis is indicated because of high rate of
bleeding from esophageal varices and the high mortality
associated with bleeding
Prophylactic Propranolol (most commonly used, 1-2mg/
kg) or Nadolol therapy are the only cost-effective ones
No role of prophylactic EST/ EVL
Prophylaxis against stress ulcers are indicated in ICU patients with any of the following charecteristics:
1) Coagulopathy/ on anti-coagulants
2) Mechanical ventilation > 2 days
3) History of GI ulceration/ bleeding within the
past year
4) Two or more of the following risk factors-
sepsis, ICU admission lasting > 1 week, occult
GI bleeding > 6 days, glucocorticoid therapy
Effective identification and antibiotic treatment of
H.Pylori infections is also crucial in preventing
complications including upper GI bleeding
Prevention of NSAID related peptic ulcer disease and
complicating UGI bleed in patients at high risk
In such patients COX-2 selective inhibitor/ non-selective
NSAID + PPI/ Misoprostol is indicated
Patients with history of uncomplicated/ complicated
PUD should be tested for H.pylori prior to beginning a
NSAID/ low dose aspirin
If H.pylori present it should be treated with appropriate
therapy, even if it is believed that PU was due to NSAIDs
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