Acute Renal Failure

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Acute Renal Failure

Transcript of Acute Renal Failure

Page 1: Acute Renal Failure

Acute Renal Failure

Page 2: Acute Renal Failure

Definition

• Sudden rise in blood urea and creatanine

• Fall in glomerular filtration rate

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Presentation

• Incidental finding on blood tests• Commonly oliguric on anuric, can be

polyuric or have normal urine volume• Symptoms of metabolic acidosis• Symptoms of salt and water overload• Haematuria• Drug overdose

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• Renal function is based on 4 sequential steps:

1. Blood flows from the renal arteries to the glomeruli

2. Glomeruli form an ultrafiltrate which flows to the renal tubules

3. Tubules reabsorb and secrete solute and/or water from the ultrafiltrate

4. Urine leaves the kidney draining into the renal pelvis, ureter and bladder, it’s then excreted through the urethra

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Classification

• Pre-renal• Renal• Post-renal

• Identifying pre and post renal causes are particularly important as they may be readily reversible

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Pre-renal

• Severe diarrhoea• Severe burns• Massive haemorrhage• Dehydration post operatively• Sepsis• Severe liver disease(hepato-renal syndrome)• Renal artery stenosis with ACEI

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Renal• Acute Hb deposition in the tubules secondary to

intravascular haemolysis• Drugs and toxins causing acute interstitial nephritis• Infection• Thromboembolic disease• Haemolytic uraemic syndrome• Thrombotic thrombocytopaeniapurpura• Malignant hypertension• Scleroderma• Vasculidities• Immune mediated

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Post-renal

• Bilateral renal calculi• Involvement of both ureters with bladder

carcinoma• Advanced cervical carcinoma• Prostatic enlargement

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Poor prognostic features

• Age >50• Septicaemia• Burns >70% surface area• Rising urea >16mmol/24hours• Oliguric >2 weeks• Multi-organ failure >3• Jaundice

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Urgent investigations• U&E• FBC and film• Coagulation• Blood cultures• Urine MC&S• ECG• CXR• USS kidneys• Consider:CK, Immunology, LDH, LFT,

HIV,HBsAg, HCVAb

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Management1. Assess state hydration-?CVP line2. Correct hypovolaemia3. Arterial pH & plasma HCO3- correct with

50-100ml 8.4% NaHCO3 slowly, centrally4. Treat hyperkalaemia (K>6.5)• If ECG abnormal-20ml 10% Ca Gluconate• Dextrose insulin infusion- 50ml 50% with

10U insulin over 30mins, thereafter 10ml/hr. BMs hourly

• Ca resonium 15g QDS orally

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5. Catheterise- does not need to remain in situ if anuric/oliguric

6. If systolic BP<100mmHg despite optimal intravascular volume start ionotropes

7. If no diuresis give hourly fluid on basis of measuring losses plus insensible losses (aprox 30ml/hour), appropriate to clinical state.

N.B. primary goal is to achieve optimal blood volume, urine flow is of secondary importance.Early mortality is often due to fluid overload and pulmonary oedema.

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8. Look for sepsis9. Stop all nephrotoxic drugs10. Give H2 blocker or PPI11. Early USS12. Consider renal biopsy if features

suggestive of multisystem disease

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Indications for dialysis

1. Life-threatening, intractable pulmonary oedema

2. Uncontrollably rising K3. Severe or worsening acidosis, pH<7.24. Uraemia

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• N.B: ARF can often be prevented

• Avoid dehydration in high risk patients e.g. :diabetics, myeloma, CRF

NBM Surgery IV contrast

• Caution with NSAIDs and aminoglycosides

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• 13 year old female• Co: acute abdominal pain• BP 100/60• U&E: Na 131

K 7.2 Ur 13 Cr 121 HCO3 8 Cl 96

• AXR: NAD• Urinalysis: glucose +++

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1. What is the most likely cause for here clinical state?

2. How would you manage here?

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• 5 year old male• CO: 2/52 bloody diarrhoea, 3/7 nausea and

malaise• OE: Periorbital oedema, BP 150/95• FBC: Hb 8 WCC 13

PLT 36• Film: anaemia, red cell fragments,

thrombocytopaenia, reticulocytosis• Clotting: PT 13s (control 13)

APTT 34s( control 36)

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• U&E: Na 138 K 5.9 Ur 11 Cr 130

1. What is the diagnosis?

2. What would you look for to confirm it?

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• 40 year old Ugandan male, found in a ditch having fallen off his boda-boda.

• Previous history of hypertension on bendrofluazide 2.5mg od, diet controlled diabetic

• OE: Drowsy, HR 41bpm, BP 140/90, Temp 36.8C, BM 9

• Cardiovascular, respiratory, abdominal examinations normal

• Left lower limb externally rotated and painful. Bruising ++++ buttock and left thigh

• FBC: Hb 9.8 WCC 14 PLT 350 MCV 84

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• Urinalysis: blood++++ Prot +

• CXR: NAD• Xray left hip: fracture dislocation NOF• ECG: minor lateral T wave changes

1. What is the diagnosis?

2. Give 2 investigations to confirm the diagnosis?

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• 30 year old female teacher from UK, returned home after visiting Uganda for 4 weeks.

• CO: Fevers, rigors, abdominal pain, headache• OE: Temp 40C, Pulse 100bpm, BP116/80, GCS

15• Cardiovascular and respiratory system NAD• Abdomen soft, 6cm tender splenomegaly• FBC: Hb 9.2

WCC 3.2 Plt 84

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• LFT: bili 56 Alp 97 ALT 29 Alb 30

• U&E: Na 131 K 5.6 Ur 16 Cr 175

• Urinalysis: blood +++ prot ++ gluc -

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1. What is the most likely cause of her illness?

2. How would you confirm the diagnosis?

3. How would you manage the patient?

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Haemolytic uraemic syndrome• Caused by E.coli 0157:H7• Most commonly from undercooked beef• Toxin causes GI effects, colicky pain, blody diarrhoea,

absent or mild fever• HUS in 6% patients with E.coli0157:H7• Characterised by MAHA, result of endothelial damage

by the toxin, causing adherence of fibrin strands, which trap fragment RBC and platlets

• Small vessel fibrin deposition and thrombosis result from MAHA causing renal damage and oliguric renal failure

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• Bruising and bleeding are common• Clotting is usually normal• Treatment is supportive• 50% need dialysis• 3-5% mortality

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RhabdomyolysisCauses:• muscle trauma/infarction• Electrocution• Hypothermia• Status epilepticus• Neuroleptic malignant syndrome• Exstacy/amphetamine abuse• Burns• Septicaemia• Statins• Very strenuous exercise (eg marathon )

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• Myoglobin is toxic to the renal tubules causing renal failure

• Serum Ca2+ drops as it is bound by the myoglobin

• K+ and PO4 increase as they are released from damaged muscle cells

Management• Hydration and alkanisation of urine• Avoid loop diuretics as they acidify the

urine

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Falciparum Malaria• Renal failure results from a combination of pyrexia,

volume depletion and haemolysis• Falciparum does not appear to cause CRFPoor prognostic signs• Neurological features; deep coma, seizures, decerebrate

posturing• Retinal haemorrhage• Hypoglycaemia• Paracitaemia>5%• Pulmonary oedema• WCC>12• Hb<7

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• DIC• Cr>250• Lactic acidosis

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• U&E: Na 135 K 6.8 Ur 16 Cr 670 HCO3 15 Ca 2.0 PO4 2.8

• LFT: Bili 14 AST 26 ALP 100 ALB 40