Hematemesis in children-Beyond Infancy
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Hematemesis in children-Beyond Infancy

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Hematemesis in children-Beyond Infancy Hematemesis in children-Beyond Infancy Presentation Transcript

  • Hematemesis in Children- Beyond Infancy
    Dr. Divya Nair
    DNB Pediatrics
    Mahavir 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
    Zollinger-Ellison syndrome 
Gastrinoma 
Results in multiple
    diffuse GI/ small bowel
    ulcerations
    Ulcer with red spot
  • Bleeding Ulcer
  • 7)Portal hypertension: 
Esophagealvarices 
Gastricvarices 
Hypertensivegastropathy
    Cirrhosis due to congenital
    hepatitis, hepatic fibrosis,
    cystic fibrosis
    8) Extra-hepatic portal vein
    obstruction
    Esophagealvarices
  • 9) Vascular malformations: 

    Hemangiomas
    Aorto-esophageal/-enteric fistulas
    Dieulafoy ulcer (superficial defect of gastric mucosa which overlies an ectaticsubmucosal a.)
    Watermelon stomach (gastric antral vascular ectasia)
    Vasculitiseg: ITP
  • 10) Tumors:
    Polyps
    Lipomas, leiomyoma
    Adenocarcinoma
    Lymphoma
    Metastatic tumors,
    Kaposi’s sarcoma, Barrett’s esophagus
    Kasabach-Merritt synd (Hemangioma thrombocytopenia
    syndrome)
  • 11) Traumatic:
Prolapsinggastropathy
    Foreign body ingestion
    Direct abdominal trauma
    Iatrogenic- throat/nose Sx,
    traumatic NG
  • 13) Miscellaneous:
    Hemobilia
    Hemosuccuspancreaticus
    Menetries’ Disease
    Eosinophilicenteropathy
    Munchausen by proxy syndrome
    Barrett’s ulcer secondary to GERD
  • B) Systemic Causes:
    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)
    Pseudoxanthomaelasticum
    KlippelTrenaunay 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 Bleeds
    MILD: 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, palmarerythema, spider nevi, gynecomastia, etc.
    Vascular malformations: hemangiomas, telangiectasias or purpura over skin
    Peutz- Jeghers syndrome: pigmented lips, palms, soles
    Pseudoxanthomaelasticum: “Plucked chicken appearance” of skin
  • Per Abdomen:
    Tenderness, Hyperactive bowel sounds
    Caput medusa with ascites, shrunken liver and
    splenomegalys/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
    InjVit 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) TransjugularIntrahepatic Porto-systemic Shunt (TIPSS):
    Percutaneous technique that creates a shunt in the
    liver between the portal & hepatic veins
    Indications: Refractory varicealh’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 withinthe
    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
  • THANK YOU