Medicine 5th year, 2nd & 3rd lectures (Dr. Kawa Husain)
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Medicine 5th year, 2nd & 3rd lectures (Dr. Kawa Husain)

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The lecture has been given on Dec. 4th & 5th, 2010 by Dr. Kawa Husain.

The lecture has been given on Dec. 4th & 5th, 2010 by Dr. Kawa Husain.

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Medicine 5th year, 2nd & 3rd lectures (Dr. Kawa Husain) Medicine 5th year, 2nd & 3rd lectures (Dr. Kawa Husain) Presentation Transcript

  • ESTABLISHED ACUTE RENAL FAILURE
    Established ARF may develop following severe or prolonged under-perfusion of the kidney (pre-renal ARF). In such cases, the histological pattern of acute tubular necrosis is usually seen.
    Acute tubular necrosis (ATN)
    Acute necrosis of renal tubular cells may result from ischaemiaor nephrotoxicity, caused by chemical or bacterial toxins, or a combination of these factors.
  • Pathogenesis of ATN
    Ischaemic tubular necrosis
    Ischaemic tubular necrosis usually follows a period of shock, during which renal blood flow is greatly reduced.
    Even when systemic haemodynamics are restored, renal blood flow can remain as low as 20% of normal, due to swelling of the endothelial cells of the glomeruli and peritubular capillaries, and oedema of the interstitium.
    Blood flow is further reduced by vasoconstrictors such as thromboxane, vasopressin, noradrenaline (norepinephrine) and angiotensin II, (partly counterbalanced by the release of intrarenal vasodilator prostaglandins). Thus, in ischaemic ATN there is reduced oxygen delivery to the tubular cells.
  • The tubular cells are vulnerable to ischaemiabecause they have high oxygen consumption in order to generate energy for solute reabsorption, particularly in the thick ascending limb of the loop of Henle.
    The ischaemic insult ultimately causes death of tubular cells , which may shed into the tubular lumen causing tubular obstruction.
    Focal breaks in the tubular basement membrane develop, allowing tubular contents to leak into the interstitial tissue and cause interstitial oedema.
  • Nephrotoxic ATN
    In nephrotoxic ATN a similar sequence occurs, but it is initiated by direct toxicity of the causative agent to tubular cells.
    Examples include the aminoglycoside antibiotics, such as gentamicin, the cytotoxic agent cisplatin, and the antifungal drug amphotericin B.
  • There are two major histiologic changes that take place in ATN:
    (1) tubular necrosis with sloughing of the epithelial cells
    (2) occlusion of the tubular lumina by casts and by cellular debris
  • Features of Established ARF
  • Features of Established ARF
    These reflect the causal condition( cause of ARF), such as bleeding,dehydration, septicaemia or systemic disease, together with features of renal failure.
    Alterations in urine volume
    Oliguric:
    Patients are usuallyoliguric (urine volume < 500 ml daily).
    Anuria :
    (complete absence of urine) is rare and usually indicates acute urinary tract obstruction or vascular occlusion.
    Normal or increased (non-oliguric ARF):
    In about 20% of cases, the urine volume is normal or increased, but with a low GFR and a reduction of tubular reabsorption.
    Excretion is inadequate despite good urine output, and the plasma urea and creatinine increase.
  • Uraemic features include initial anorexia, nausea and vomiting followed by drowsiness, apathy, confusion, muscle-twitching, hiccoughs, fits and coma.
    ,
    Respiratory rate may be increased due to acidosis, pulmonary oedemaor respiratory infection.
    Pulmonary oedema may result from the administration of excessive amounts of fluids relative to low urine output and because of increased pulmonary capillary permeability.
    Anaemiadue to excessive blood loss or haemolysis .
    Bleedingis more likely because of disordered platelet function and disturbances of the coagulation cascade.
  • Retention of salt and water
    Pulmonary edema, peripheral edema, ascites, pleural effusion
    Spontaneous gastrointestinal haemorrhage
    may occur, often late in the illness, although this is less common with effective dialysis and the use of agents that reduce gastric acid production.
    Infections( may be severe )
    may complicate ARF because humoraland cellular immune mechanisms are depressed.
    pericarditis
  • Disturbances of water, electrolyte and acid-base balance
    Hyperkalaemia is common, particularly with massive tissue breakdown, haemolysis or metabolic acidosis
    Dilutionalhyponatraemiaoccurs if the patient has continued to drink freely despite oliguria or has received inappropriate amounts of intravenous dextrose.
    Metabolic acidosis develops unless prevented by loss of hydrogen ions through vomiting or aspiration of gastric contents.
    Hypocalcaemia, due to reduced renal production of 1,25-dihydroxycholecalciferol, is common.
  • Managementof Established ARF
  • Managementof Established ARF
    Emergency resuscitation
    Hyperkalaemia(a plasma K+ concentration > 6 mmol/l) must be treated immediately, to prevent the development of life-threatening cardiac arrhythmias.
    Hypovolaemia must be treated as for reversible pre-renal ARF , with monitoring of central venous or pulmonary wedge pressure as required.
    Circulating blood volume should be optimised to ensure adequate renal perfusion .
    In an anuric or volume-overloaded patient, renal replacement therapy may be required ( dialysis ).
    Patients with pulmonary oedemausually require dialysis to remove sodium and water.
    Severe acidosis can be ameliorated with isotonic sodium bicarbonate (e.g. 500 ml of 1.26%) if volume status allows.
  • The underlying cause of the ARF
    This may be obvious or revealed by simple initial investigations (e.g. ultrasound showing urinary tract obstruction). If not, a range of investigations, including renal biopsy, may be necessary .
    There is no specific treatment for ATN, other than restoring renal perfusion.
    Intrinsic renal disease may require specific therapy; for example, immunosuppressive drugs are of value in some causes of rapidly progressive glomerulonephritis and plasma infusion and plasma exchange may be indicated in microangiopathic diseases .
    Post-renal' obstruction should be relieved urgently.
    If pelvic or ureteric dilatation is found and not explained by bladder outlet obstruction, percutaneousnephrostomyis undertaken to decompress the urinary system .
    With rapid intervention, dialysis can usually be avoided.
  • Fluid and electrolyte balance
    After initial resuscitation, daily fluid intake should equal urine output, plus an additional 500 ml to cover insensible losses; such losses are higher in febrile patients and in tropical climates.
    If abnormal losses occur, as in diarrhoea, additional fluid and electrolyte replacement is required.
    Measurement of fluid intake and urine output is subject to error so the patient should be weighed daily.
    Large changes in body weight, the development of oedema or signs of fluid depletion indicate that fluid intake should be reassessed.
    Since sodiumand potassium are retained, intake of these substances should be restricted
  • .
    Protein and energy intake
    In patients in whom dialysis is likely to be avoided, accumulation of urea is slowed by dietary proteinrestriction (to about 40 g/day) and by suppression of protein catabolism by giving as much energy as possible in the form of fat and carbohydrate.
    Patients treated by dialysis may have more dietary protein (70 g protein daily). It is important to give adequate energy and nitrogen to hypercatabolic patients (e.g. sepsis, burns).
    In some patients, feeding via a nasogastric tube may be helpful.
    Parenteral nutrition may be required, especially in critically ill patients, because of vomiting or diarrhoea, or if the bowel is not intact.
    Infection control
    Patients with ARF are at risk of intercurrent infection. Regular clinical examination and microbiological investigation, as clinically indicated, are required to diagnose and treat this complication promptly.
  • Dietary modification
    total caloric intake– 35~ 50 kcal/kg/day
    to avoid catabolism
    Salt restriction– 2~4 g/day
    Potassium intake– 40 meq/day
    Phosphorus intake– 800 mg/day
    Carbohydrate ≥ 100gm/day to minimize ketosis and protein catabolism
  • Drugs
    Some drugs such as NSAIDs and ACE inhibitors may prolong ARF and temporary withdrawal should be considered.
    Many drugs are excreted renally and dose adjustment may be required in ARF to avoid accumulation.
    Renal replacement therapy
    This may be required as supportive management in ARF
  • RENAL REPLACEMENT IN ACUTE RENAL FAILURE ( dialysis )
    • Hyperkalaemia. A plasma potassium > 6 mmol/l is hazardous. Elevated plasma potassium can usually be reduced by medical measures in the short term , but dialysis is often required for definitive control.
    • Metabolic acidosis. This will often occur together with hyperkalaemia and raise the plasma potassium further.
    • Fluid overload and pulmonary oedema. In patients with continued urine output, this may be controlled by careful fluid balance and use of diuretics, but in oligo/anuric patients may be an indication for RRT.
    • Uraemicpericarditis/uraemic encephalopathy. These are features of severe untreated renal failure; they are uncommon in ARF but are strong indications for RRT.
    • Drug resistant GI manifestations ( repeated vomiting )
  • Absolute indication
    • CCr 5 ml/min or serum Cr  10.0 mg/dl
    Relative indication
    • CCr 10 ml/min or serum Cr  8.0 mg/dl
    • With accompanied symptoms or signs
    = CHF/Pulmonary edema = Uremic pericarditis= Bleeding tendency = Neurologic symptoms= Drug-resistant hyper-K = Drug-resistant metabolic acidosis = Drug-resistant nausea/vomiting
    Indication of Dialysis
  • The options for renal replacement therapy in ARF are :HaemodialysisHigh-volume haemodialysisContinuous arteriovenous or venovenoushaemofiltrationPeritoneal dialysis
  • Recovery from ARF
    Fortunately, tubular cells can regenerate and re-form the basement membrane.
    If the patient is supported during the regeneration phase, kidney function usually returns.
    During recovery some patients, primarily those with ATN or after relief of chronic urinary obstruction, develop a 'diuretic phase in which urine output increases rapidly and remains excessive for several days before returning to normal.
    This is due in part to loss of the medullary concentration gradient, which normally allows concentration of the urine in the collecting duct.
    d the rate of recovery
  • Fluid should be given to replace the urine output as appropriate.
    Supplements of sodium chloride, sodium bicarbonate and potassium chloride, and sometimes calcium, phosphate and magnesium, may be needed to compensate for increased urinary losses.
    After a few days urine volume falls to normal as the concentrating mechanism and tubular reabsorption are restored.
    Not all patients have a diuretic phase, depending on the severity of the renal damage and the rate of recovery
  • Prognosis of ARF
    In uncomplicated ARF, such as that due to simple haemorrhage or drugs, mortality is low even when renal replacement therapy is required.
    In ARF associated with serious infection and multiple organ failure, mortality is 50-70%.
    Outcome is usually determined by the severity of the underlying disorder and other complications, rather than by renal failure itself.
  • urine and serum laboratory values
  • acute renal failure:diagnosis
    • History and Physical examination
    • Blood tests : CBC, BUN/creatinine, electrolytes, uric acid, PT/PTT, CK
    • Urine analysis
    • Renal Indices
    • Renal ultrasound (useful for obstructive forms)
    • Doppler (to assess renal blood flow)
    • Nuclear Medicine Scans
  • renal indices
    Reabsorption of water and sodium:
    - intact in pre-renal failure
    - impaired in tubulo-interstitial disease and ATN
    Since urinary indices depend on urine sodium concentration, they should be interpreted cautiously if the patient has received diuretic therapy
  • renal indices
    Renal Failure Index (RFI)
    RFI: urine [Na]
    urine creatinine / serum creatinine
  • renal indices
    Fractional Excretion of Na (FENa)
    FENa: [ urine Na/serum Na] x 100 %
    [urine creatinine/serum creatinine]
  • prerenalARF:
    Urine sediment: hyaline and fine granular casts
    Urinary to plasma creatinine ratio: high
    Urinary Na: low
    FENa: low
    Increased urine output in response to hydration
  • renal ARF:
    Urine sediment: brown granular casts and tubular epithelial cells
    Urinary to plasma creatinine ratio: low
    Urinary Na: high
    FENa: high
  • Serum BUN/creatinine ratio — 
    In adults and older children, the serum BUN/creatinine ratio is normal at 10 to 15:1 in ATN, and may be greater than 20:1 in prerenal disease due to the increase in the passive reabsorption of urea that follows the enhanced proximal transport of sodium and water. Thus, a high ratio is highly suggestive of prerenal disease.
  • Urine osmolality —
     Loss of concentrating ability is an early and almost universal finding in ATN with the urine osmolality usually being below 350 mosmol/kg.
    In contrast, a urine osmolality above 500 mosmol/kg is highly suggestive of prerenal disease.
  • Fractional excretion of sodium (FENa) — 
    The effect of variations in urine volume can be eliminated by calculating the FENa
                                            UNa   x   PCr
             FENa (percent)    =       — — — — — — — — —     x    100
                                            PNa   x   UCr
    where UCr and PCr are the urine and serum creatinine concentrations, respectively, and UNa and PNa are the urine and serum sodium concentrations, respectively.
    The FENa is a screening test that differentiates between prerenal AKI and ATN .
    A value below 1 percent suggests prerenal disease, where the reabsorption of almost all of the filtered sodium represents an appropriate response to decreased renal perfusion.
    A value between 1 and 2 percent may be seen with either disorder.
    A value above 2 percent usually indicates ATN.