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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

ER conference

Co* Concepcion * Conti * Corpuz * Cosico * Cruz * Cruz


General data

General Data

  • 10-month-old, Female

  • From Isabela

Chief Complaint:

Pallor and anuria for 2 days


History of present illness

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


History of present illness1

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


History of present illness2

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


Family history

Family History

  • (-) kidney disease


Physical examination

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


Other pertinent information

Other pertinent information

  • blahblah


Approach to diagnosis

Approach to Diagnosis


Salient features

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


Presenting manifestation

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.


Presenting manifestation1

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.


Differential diagnosis

Differential Diagnosis


Impression hemolytic uremic syndrome

Impression:Hemolytic Uremic Syndrome


Hemolytic uremic syndrome hus

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


Hemolytic uremic syndrome hus1

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


Types of hus

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


Types of hus1

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


Clinical manifestation

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


Clinical manifestation1

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


Clinical course

Clinical Course

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


Pathogenesis

Pathogenesis


Pathogenesis1

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.


Summary of the pathophysiology

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


Microangiopathic hemolytic anemia

Microangiopathic hemolytic anemia


Microangiopathic hemolytic anemia1

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


Thrombocytopenia

Thrombocytopenia


Thrombocytopenia1

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


Acute renal injury

Acute Renal Injury


Acute kidney injury

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)


Rifle criteria

Rifle Criteria


Er conference

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


Er conference

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


Er conference

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


Etiology of acute renal failure

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


Urinalysis urine chemistries and osmolality in acute renal failure

Urinalysis, Urine Chemistries, and Osmolality in Acute Renal Failure

Kliegman: Nelson Textbook of Pediatrics, 18th ed.


Complications of aki

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.


Complications of aki1

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)

Kliegman: Nelson Textbook of Pediatrics, 18th ed.


Complications of aki2

Complications of AKI

  • 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.


Complications of aki3

Complications of AKI

  • Uremia

    • Accumulation of nitrogenous wastes w/c are normally excreted in the urine

    • Occurs in GFR <50%

    • Early symptoms: anorexia and lethargy

    • Late symptoms: decreased mental acuity and coma


Other systems involved

Other Systems Involved


Other systems involved1

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.


Other systems involved2

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


Diagnostics

Diagnostics


Diagnosis

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


Diagnosis1

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.


What labs can we request for our patient

What labs can we request for our patient

  • CBC with platelet count

  • Reticulocyte count

  • Peripheral smear

  • Urinalysis

  • PT, aPTT

  • Serum electrolytes

  • Creatinine

  • Blood culture

  • Stool culture


What labs can we request for our patient1

What labs can we request for our patient

  • CBC with platelet count

    • Hemoglobin=5-9 g/dL

    • White blood cell count may rise to 30.000/mm3

      • Magnitude related to severity and prognosis of the syndrome

    • Thrombocytopenia (20.000 - 100.000/mm3) occurs in more than 90% of patients.


What labs can we request for our patient2

What labs can we request for our patient

  • Reticulocyte count

    • Reticulocyte count is moderately elevated


What labs can we request for our patient3

What labs can we request for our patient

  • Peripheral smear

    • Helmet cells, burr cells and fragmented red blood cells


What labs can we request for our patient4

What labs can we request for our patient

  • Urinalysis

    • microscopic hematuria and proteinuria


What labs can we request for our patient5

What labs can we request for our patient

  • PT, aPTT

    • Usually within normal range however may also show prolonged bleeding time.


What labs can we request for our patient6

What labs can we request for our patient

  • Serum electrolytes

    • Hyperkalemia

    • Hyperphosphatemia

    • Hypocalcemia

    • Metabolic acidosis


What labs can we request for our patient7

What labs can we request for our patient

  • BUN, Creatinine

    • Markedly elevated BUN and creatinine


What labs can we request for our patient8

What labs can we request for our patient

  • Stool culture

    • Typically detect shiga toxin-producing E coli

  • Blood culture

    • Negative


Treatment

Treatment


Treatment1

Treatment

  • Current treatment of STEC induced HUS targets gastrointestinal, hematologic, vascular and renal complications.

    • It includes isotonic volume replacement or expansion, red blood cell and platelet transfusion and, for severe AKI, hemo- or peritoneal dialysis

Kidney International (2009) 75, S62–S66; doi:10.1038/ki.2008.624

Treatment options for HUS secondary to Escherichia coli O157:H7

1Division of Nephrology, Montreal Children's Hospital and McGill University, Montreal, Quebec, Canada

Correspondence: Martin Bitzan, Division of Nephrology, Montreal Children's Hospital, 2300, rue Tupper – E222, Montreal, Quebec, Canada H3H 1P3.

Nelson’s Textbook of Pediatrics, 18th edition


Treatment2

Treatment

  • Supportive care with meticulous attention to

    • Anemia

    • Thrombocytopenia

    • AKI and complications

      • Fluid and electrolytes

      • Hypertension

      • Uremia

Bihar Pedicon 2006 - Conference Abstracts.PediatricOncall [serial online] 2006 [cited 15 September 2006(Supplement 9)];3.

Wong CS, Jelacic S, Habeeb RL, Watkins SL, Tarr PI: The risk of the hemolytic-uremic syndrome after antibiotic treatment of Escherichia coli O157:H7 infections. N Engl J Med 342 : 1930 –1936, 2000


Anemia

Anemia

  • packed red blood cells (RBC) should be transfused when the hemoglobin (Hgb) level is <7 g/dL or hematocrit <18

  • About 80 percent of patients w/ HUS require PRBC transfusions

    guidelines for children >4 months of age are similar to those used in adults. In general, RBC transfusion is recommended for Hgb levels <7 g/dL, since most such children become symptomatic with malaise, irritability, and/or lassitude

Teruya, Jun (2009). Indications for RBC transfusion in infants and children. Uptodate 17.1 Desktop


Thrombocytopenia2

Thrombocytopenia

  • Platelet transfusion is reserved for patients with HUS who have significant clinical bleeding or if an invasive procedure is required.

  • Rare bec platelet count rarely <10,000/mm3

    based upon unsubstantiated concerns that consumption of infused platelets would contribute to new or expanding thrombi as reported in adults with thrombotic thrombocytopenic purpura

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


Fluids

Fluids

  • Fluid management is based upon the intravascular fluid status of the patient and renal function.

    • Decreased intravascular volume are repleted to an euvolemic state.

    • Increased volume and diminished urine output are fluid restricted.

      • Diuretics rarely avert anuria but a trial of furosemide (2 to 5 mg/kg per dose) may be attempted to induce a diuresis

      • Dialysis therapy is required if fluid restriction and/or diuretic therapy fail

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


Fluids1

Fluids

  • Once the patient is in an euvolemic state, administration of fluids should be given as insensible losses plus urine output until renal function returns to normal

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


Electrolytes

Electrolytes

  • Common due to acute kidney injury/failure

    • Hyperkalemia

    • Hyperphosphatemia

    • Metabolic acidosis

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


Electrolytes1

Electrolytes

  • Hyperkalemia

    • Stabilization of the cardiac membrane with the intravenous calcium (calcium gluconate 10 percent solution in a dose 0.5 to 1.0 mL per kilogram intravenously over 5 to 15 minutes).

    • Promotion of potassium movement from the extracellular fluid (ECF) into the cells via three different therapies:

      • Glucose and insulin (0.5 to 1.0 g of glucose per kilogram over 30 minutes and 0.1 unit of insulin per kilogram intravenously or subcutaneously);

      • intravenous sodium bicarbonate (in a dose of 1 to 2 milliequivalent per kilogram over 30 to 60 minutes);

      • beta agonists, such as albuterol, via nebulization (2.5 mg if the child weighs less than 25 kilogram or 5 mg if the child weighs more).

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


Electrolytes2

Electrolytes

  • Hyperphosphatemia and hypocalcemia

    • Oral phosphate binders and dietary restriction of phosphorus are commonly used to decrease intestinal absorption of phosphorus.

    • Intravenous administration of calcium gluconate should be considered if hypocalcemia is severe and/or if bicarbonate therapy is required for severe acidosis and hyperkalemia

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


Electrolytes3

Electrolytes

  • Acidosis

    • Due to inability to excrete acid.

    • Patients with serum bicarbonate levels that are above 14 mEq/L or with arterial pH greater than 7.2 do not require intervention.

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


Dialysis

Dialysis

  • 2/3 of HUS patients will require dialysis

  • Indications for dialysis include the following:   

    • Volume overload with evidence of hypertension and/or pulmonary edema refractory to diuretic therapy   

    • Persistent hyperkalemia

    • Severe metabolic acidosis unresponsive to medical management   

    • Neurologic symptoms (altered mental status, seizures)   

    • Blood urea nitrogen greater than 100–150 mg/dL (or lower if rapidly rising)   

    • Calcium/phosphorus imbalance, with hypocalcemictetany

    • Inability to provide adequate nutritional intake because of the need for severe fluid restriction

Kliegman: Nelson Textbook of Pediatrics, 18th ed.


Dialysis1

Dialysis

  • Peritoneal dialysis may contribute to the dissolution of vascular thrombi by removing fibrinolysis inhibitors and circulating plasminogen activating inhibitor-1, thereby activating normal endogenous fibrinolytic pathways.

Nelson’s Textbook of Pediatrics, 18th edition


Hypertension

Hypertension

  • caused by overexpansion of intravascular volume and/or ischemia-induced activation of the renin-angiotensin system

    • calcium channel blockers (such as nifedipine or nicardipine) as the initial choice of antihypertensive

    • changed to ACE inhibitors in patients who appear to have long-term renal sequelae

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


Prevention

Prevention


Antibiotics

Antibiotics

  • Prevention of HUS by antibiotic therapy to treat E.coli intestinal infection or early HUS is a very controversial subject.

    • antibiotic therapy at the stage of gastrointestinal infection with Stx-E. coli increases—by approximately 17-fold—the risk for full-blown HUS. I

      • antibiotic-induced injury to the bacterial membrane might favor the acute release of large amounts of toxins.

    • Other reports failed to show a higher risk for HUS associated with antibiotic administration.

      On the basis of available data, we suggest that in patients with Stx-E. coli gastrointestinal infection, antibiotics should be avoided unless in cases with sepsis.

Scheiring J, Andreoli SP and Zimmerhackl LB. Treatment and outcome of Shiga-toxin-associated hemolytic uremic syndrome (HUS). PediatrNephrol (2008) 23:1749–1760


Anti motility agents

Anti-motility agents

  • In children with hemorrhagic colitis due EHEC infection, the use of antimotility agents has been associated with a greater risk for developing HUS. Thus, antidiarrheal agents are usually avoided

    • contributes to retention of Stx within the colon, which could enhance absorption of the toxin

Scheiring J, Andreoli SP and Zimmerhackl LB. Treatment and outcome of Shiga-toxin-associated hemolytic uremic syndrome (HUS). PediatrNephrol (2008) 23:1749–1760


Thank you

THANK YOU 


Peritoneal dialysis pd vs intermittent hemodialysis ihd vs continual renal replacement therapy crrt

Peritoneal Dialysis (PD) vs Intermittent Hemodialysis (IHD) vs Continual Renal Replacement Therapy (CRRT)

PD IHC CRRT

BENEFITS      

  • Fluid removal + ++ ++

  • Urea and creatinine clearance + ++ +

  • Potassium clearance ++ ++ +

  • Toxin clearance + ++ +

    COMPLICATIONS      

  • Abdominal pain + - -

  • Bleeding - + +

  • Dysequilibrium - + -

  • Electrolyte imbalance ++ +

  • Need for heparinization - + +

  • Hyperglycemia + - -

  • Hypotension + ++ +

  • Hypothermia - - +

  • Central line infection - + +

  • Inguinal/abdominal hernia + - -

  • Peritonitis + - -

  • Protein loss + - -

  • Respiratory compromise + - -

  • Vessel thrombosis - + +

Nelson’s Textbook of Pediatrics, 18th edition


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