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ER conference

ER conference. Co* Concepcion * Conti * Corpuz * Cosico * Cruz * Cruz . General Data. 10-month-old, Female From Isabela. Chief Complaint: Pallor and anuria for 2 days. History of Present Illness. 8 days PTA. Loose, blood-streaked, mucoid , greenish stools 4-5 x per day

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ER conference

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  1. ER conference Co* Concepcion * Conti * Corpuz * Cosico * Cruz * Cruz

  2. General Data • 10-month-old, Female • From Isabela Chief Complaint: Pallor and anuria for 2 days

  3. History of Present Illness 8 days PTA • Loose, blood-streaked, mucoid, greenish stools • 4-5 x per day • ~1 cup per episode • Associated with vomiting of previously ingested milk • Good urine output • Brought to a private doctor • Advised ORS after each bowel movement • Metronidazole 30mg/kg/day

  4. History of Present Illness 3 days PTA • 1 episode of bowel movement • Non-blood streaked, formed stools • no vomiting • Decrease in urine output • Highly colored urine

  5. History of Present Illness 1 day PTA • 5 episodes of vomiting • Pallor • No urine output • Brought back to private doctor • Referred to USTH for further management Transfer to ustH

  6. Family History • (-) kidney disease

  7. Physical Examination • Irritable but not in respiratory distress • Vital signs were as follows: • BP 90/60 mmHg • Anthropometric measurements : • Lt : 75 cm (p75) Wt : 10 kg (p75) • Pale, dry skin and petechial rash on the abdomen • Anterior fontanel and eyeballs slightly sunken • Liver – palpable 3 cm below RSCM • Liver span 6cm • Urinary bladder not palpable • Strong peripheral pulses • No signs of edema

  8. Other pertinent information • blahblah

  9. Approach to Diagnosis

  10. Salient Features Subjective Objective • 10 mo old/F • Diarrhea • Vomiting • Anuria • Pallor • Signs of dehydration • Slightly sunken fontanelles and eyeballs • Irritability • Dry skin • Petechial rash • Hepatomegaly? • Strong pulses

  11. Presenting Manifestation • Look for a symptom, sign or laboratory finding.. • Pathognomonic of a disease • Pointing to an organ or part of an organ • Pointing to a group of disease • Mechanism is well understood • Found in the least number of diseases UST: Pedia (2009). Guideline for History Taking, PE and Diagnosis of Pediatric Patients. 2nd ed.

  12. Presenting Manifestation • Look for a symptom, sign or laboratory finding.. • Pathognomonic of a disease • Pointing to an organ or part of an organ • Pointing to a group of disease • Mechanism is well understood • Found in the least number of diseases “GI: Vomiting and diarrhea and w/ signs of dehydration Renal: anuria Petechial rash” UST: Pedia (2009). Guideline for History Taking, PE and Diagnosis of Pediatric Patients. 2nd ed.

  13. Differential Diagnosis

  14. Impression:Hemolytic Uremic Syndrome

  15. Hemolytic uremic syndrome (HUS) • One of the main causes of AKI in children under 3 years of age and an important cause of chronic renal failure and shock during youth • Classical triad: • Microangiopathic hemolytic anemia • Thrombocytopenia • Acute kidney injury Niaudet, Patrick (2009). Clinical Manifestation and diagnosis of Shiga-like toxin associated (typical) Hemolytic Uremic Syndrome in children. Uptodate 17.1 desktop

  16. Hemolytic uremic syndrome (HUS) • 90% of cases are preceded by a prodrome of bloody diarrhea • toxin-mediated endothelial cell damage, resulting in thrombotic microangiopathy and intraluminal thrombosis of small vessels, with subsequent tissue ischemia and necrosis Niaudet, Patrick (2009). Clinical Manifestation and diagnosis of Shiga-like toxin associated (typical) Hemolytic Uremic Syndrome in children. Uptodate 17.1 desktop

  17. Types of HUS • Shiga-like toxin associated HUS (90%) • Aka typical, classical, or diarrhea-associated HUS • Escherichia coli and type 1 Shigelladysenteriae • EnterohemorrhagicE. coli (EHEC) produces a toxin called verotoxinand accounts for 70% of post-diarrheal HUS • 80% of EHEC are caused by E. coli O157:H7 • Shigelladysenteriae type 1: more severe HUS Niaudet, Patrick (2009). Clinical Manifestation and diagnosis of Shiga-like toxin associated (typical) Hemolytic Uremic Syndrome in children. Uptodate 17.1 desktop

  18. Types of HUS • Non-shiga-like toxin associated HUS (10%) • aka atypical, nondiarrhea-associated HUS • absence of diarrhea or Shiga toxin-producing E. coli infection • Most commonly due to Strep pneumoniae • Prodromal features of URTI, fever or vomiting Niaudet, Patrick (2009). Clinical Manifestation and diagnosis of Shiga-like toxin associated (typical) Hemolytic Uremic Syndrome in children. Uptodate 17.1 desktop

  19. Clinical Manifestation • Prodromal illness with abdominal pain, vomiting and diarrhea immediately precedes HUS • Prodromal diarrhea was present in 91% • Diarrhea was bloody in 57% of cases • Vomiting occurs in 30 to 60% of cases • Fever occurs in 30%. • HUS begins 5-10 days after the onset of diarrhea. There is sudden onset of: • Anemia (microangiopathic hemolytic anemia) • Thrombocytopenia • Acute Renal injury

  20. Clinical Manifestation • Early symptoms: • Blood in the stools • Irritability • Fever • Lethargy and Weakness • Vomiting and diarrhea • Later symptoms • Bruising/Skin rash that looks like fine red spots (petechiae) • Jaundice • Decreased consciousness • Oliguria/Anuria • Pallor • Seizures

  21. Clinical Course Niaudet, Patrick (2009). Clinical Manifestation and diagnosis of Shiga-like toxin associated (typical) Hemolytic Uremic Syndrome in children. Uptodate 17.1 desktop

  22. Pathogenesis

  23. Pathogenesis • The primary event in pathogenesis of the syndrome appears to be endothelial cell injury. • Capillary and arteriolar endothelial injury in the kidneys leads to localized clotting. • The microangiopathic anemia results from mechanical damage to the red blood cells as they pass to the altered vasculature. • Thrombocytopenia is due to intrarenal platelet adhesion or damage.

  24. Summary of the Pathophysiology Ingestion of EHEC containing shiga toxin Attaches to endothelial lining Damage Inflammation Circulatory system Cytokines TNF a IL-8 RBC Platelet WBC Apoptosis Hemolytic anemia Hemolysis Platelet aggregation Consumptive thrombocytopenia Pallor Microthrombi Petechiae Highly colored urine Deposited in various organs particularly Kidney

  25. Microangiopathic hemolytic anemia

  26. Microangiopathic hemolytic anemia • endothelial cell injury  leading to intravascular coagulation, fibrin deposition, and platelet adherence to microthrombi within the vascular lumen  Altered blood flow  results in red blood cell destruction. • Low hemoglobin • Negative coomb’s test • Peripheral blood smear • schistocytes (up to 10 percent of red cells) Tzipori S, Sheoran A, Akiyoshi D, Donohue-Rolfe A, and Trachtman H. Antibody Therapy in the Management of Shiga Toxin-Induced Hemolytic Uremic Syndrome. Clinical Micro Reviews, 2004 V17 No4, p. 926–941

  27. Thrombocytopenia

  28. Thrombocytopenia • platelet count below 140,000/mm3 and usually about 40,000/mm3. • Despite this, there is usually no purpura or active bleeding Niaudet, Patrick (2009). Clinical Manifestation and diagnosis of Shiga-like toxin associated (typical) Hemolytic Uremic Syndrome in children. Uptodate 17.1 desktop

  29. Acute Renal Injury

  30. Acute Kidney Injury • clinical syndrome in which a sudden deterioration in renal function results in the inability of the kidneys to maintain fluid and electrolyte homeostasis • Present in 55-70% of HUS • renal function recoversin most of them (up to 70% in various series)

  31. Rifle Criteria

  32. Barlettaa, G.M.& Bunchman T.E. Acute renal failure in children and infants. CurrOpinCrit Care 10:499–504., 2004

  33. Barlettaa, G.M.& Bunchman T.E. Acute renal failure in children and infants. CurrOpinCrit Care 10:499–504., 2004

  34. Barlettaa, G.M.& Bunchman T.E. Acute renal failure in children and infants. CurrOpinCrit Care 10:499–504., 2004

  35. Etiology of Acute Renal Failure Biljon, GV. Causes, Prognostic Factors and Treatment Results of Acute Renal Failure in Children Treated in a Tertiary Hospital in South Africa. Journal of Tropical Pediatrics Vol. 54, No. 4, 13 March 2008

  36. Urinalysis, Urine Chemistries, and Osmolality in Acute Renal Failure Kliegman: Nelson Textbook of Pediatrics, 18th ed.

  37. Complications of AKI • Hyponatremia • Most common cause is accumulation of fluid in excess of solute • Hyperkalemia • Result of the inability to excrete quantitatively the potassium derived from the diet, as well as that released from catabolism, necrotic tissue, and hemolyzed erythrocytes • Hypocalcemia &Hyperphosphatemia • Almost constant early finding in ARF • Due to phosphate retention, coupled with release of phosphate from tissue breakdown, contribute to the depression of the serum calcium concentration Kliegman: Nelson Textbook of Pediatrics, 18th ed.

  38. Complications of AKI • Metabolic Acidosis • May occur via 3 basic mechanisms:    • Loss of bicarbonate from the body    • Impaired ability to excrete acid by the kidney    • Addition of acid to the body (exogenous or endogenous) • Hypertension • May result from hyperreninemia associated with the primary disease process and/or expansion of the extracellular fluid volume and is most common in ARF patients with acute glomerulonephritis or HUS Kliegman: Nelson Textbook of Pediatrics, 18th ed.

  39. Complications of AKI • Uremia • Accumulation of nitrogenous wastes w/c are normally excreted in the urine • Occurs in GFR <30% • Early symptoms: anorexia,vomitingand lethargy • Late symptoms: decreased mental acuity and coma

  40. Other Systems Involved

  41. Other Systems involved • Central nervous system (20%): seizures, coma, stroke, hemiparesis, and cortical blindness. Severe CNS involvement is associated with increased mortality. • Gastrointestinal tract: Any area from the esophagus to the perianal area can be involved. The more serious manifestations include severe hemorrhagic colitis, bowel necrosis and perforation, rectal prolapse, peritonitis, and intussusception. • Cardiac dysfunction: Cardiac dysfunction can be due to cardiac ischemia detected by elevated levels of troponin I, uremia, and fluid overload.

  42. Other Systems involved • Pancreas: transient diabetes mellitus may occur, and rarely permanent diabetes mellitus, which may develop years later. • Liver: Hepatomegaly and/or increased serum transaminases are frequent findings. • Hematology: In addition to anemia and thrombocytopenia, leukocytosis is common in diarrhea-induced HUS; the prognosis is worse with increased white blood cell counts

  43. Diagnostics

  44. Diagnosis • Based on presenting signs and symptoms. • The classic diagnostic criteria: • microangiopathic hemolytic anemia • thrombocytopenia • acute renal failure • Followed by an episode of bloody diarrhea • Physical Examination may show: • Hepatomegaly/ Splenomegaly • Neurologic changes

  45. Diagnosis • Laboratory tests: • Blood clotting tests (PT and PTT) • BUN and creatinine • Complete blood count • Platelet count • Urinalysis • Urine protein • Other tests: • Kidney biopsy • Stool culture McMillan R. Hemorrhagic disorders: abnormalities of platelet and vascular function. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 179.

  46. What labs can we request for our patient • CBC with platelet count • Peripheral smear • Urinalysis • Serum electrolytes • Creatinine • Stool culture

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