What is Medicine - Acute Kidney Injury
A sudden decline in kidney function is characterised by one of the following (1): Serum creatinine (SCr) increases by 0.3 mg/dL within 48 hours, by 50% within 7 days, and by 0.5 mL/kg/hr for >6 hours. This causes anomalies in volume, acid-base, and electrolyte balance as well as retention of nitrogenous waste. EPIDEMIOLOGY Incidence Acute kidney damage (AKI) accounts for 5% of hospital admissions and 30% of ICU admissions. AKI occurs in 25% of hospitalised patients; 50% of these cases are iatrogenic. A >4-fold greater risk of death is linked to developing AKI while an inpatient. PATHOPHYSIOLOGY AND AETIOLOGY Prerenal, intrarenal, and postrenal are the three groups. Reduced renal perfusion caused by prerenal (usually reversible): - Glomerular filtration rate (GFR) decreases as a result of decreased renal perfusion, which is frequently brought on by hypovolemia. caused by renal artery stenosis/embolism, hypotension, volume depletion (GI losses, excessive sweating, diuretics, haemorrhage), burns, and heart/liver failure - If the reduced perfusion persists or becomes severe, ischemic acute tubular necrosis (ATN) may result. Intrarenal (intrinsic kidney damage, frequently caused by protracted or severe renal hypoperfusion) - Acute tubular necrosis (ATN), which can be brought on by radiographic contrast material, aminoglycosides, nonsteroidal anti-inflammatory medications (NSAIDs), or other nephrotoxic chemicals. Glomerulonephritis (GN), acute interstitial nephritis (AIN; drug-induced), arteriolar insults, vasculitis, accelerated hypertension, cholesterol embolisation (after an intra-arterial operation), intrarenal deposition/sludging (uric acid nephropathy, multiple myeloma [Bence Jones proteins]), and Postrenal obstruction of the collecting system can be caused by extrinsic compression (such as benign prostatic hypertrophy [BPH], carcinoma, pregnancy), intrinsic obstruction (such as calculi, tumours, clots, strictures, and sloughed papillae), and decreased function (such as neurogenic bladder). Genetics No genetic pattern is known. RISK FACTORS Include diabetes mellitus, hypertension, heart failure, liver failure, and chronic kidney disease (CKD). Age and intravascular radiocontrast substance exposure NSAIDs, ACEIs, ARBs, and cyclosporine/tacrolimus are examples of drugs that interfere with the autoregulation of GFR. Nephrotoxic drugs include antibiotics called aminoglycosides and platinum-based chemotherapy. Hypovolemia (due to, for example, diuretics, bleeding, and GI losses) BPH; cancer (such as multiple myeloma); sepsis; surgery; rhabdomyolysis; solitary kidney (risk in nephrolithiasis); GENERAL PREVENTION Maintain adequate renal perfusion with isotonic fluids and, if required, vasopressor assistance. Avoid nephrotoxic substances, such as IV contrast, herbal supplements, and recognised nephrotoxic drugs. CONDITIONS OFTEN ASSOCIATED WITH : Drug reactions, sepsis, severe trauma, burns, transfusion reactions, recent chemotherapy, rhabdomyolysis, internal bleeding, dehydration, hyperkalemia, hyperphosphatemia, hypercalcemia, hyperuricemia, hydronephrosis, BPH, nephrolithiasis, uremic pericarditis, cirrhosis, CKD, malignant hypertension, and vasculitis. AKI typically causes no symptoms until the patient has suffered a severe loss of function. Oliguria is a potential symptom, however it is neither sensitive nor specific. HISTORY Track changes in body weight, urine output, and oral intake. A complete drug history Prerenal: symptoms of orthostasis and thirst Nephrotoxic medicines, radiocontrast material, and other poisons intrarenally Postrenal: colicky flank pain radiating to the groyne suggests ureteric obstruction, such as a stone; nocturia, frequency, and hesitancy suggest prostatic disease; suprapubic and flank pain are typically secondary to collecting system and bladder distension; anticholinergic medications prevent bladder emptying. Lethargy, nausea/vomiting, anorexia, pruritus, restless legs, disturbed sleep, and hiccups are uremic symptoms. Despite having adequate pulses, ischemic fingers, SC nodules, and livedo reticularis point to atheroembolization. An occluded renal artery or vein may be the cause of flank pain. Prerenal signs include tachycardia, decreased jugular venous pressure (JVP), orthostatic hypotension, dry mucous membranes, and decreased skin turgor. Uremic signs include altered sensorium, seizures, asterixis, myoclonus, pericardial friction rub, and peripheral neuropathies. A pruritic rash, livedo reticularis, SC nodules, and ischemia fingers despite normal pulses are examples of intrinsic renal symptoms. Postrenal signs include suprapubic distension, flank pain, and an enlarged prostate. DETECTION & INTERPRETATION OF DIAGNOSIS Initial examinations (lab, imaging) Contrast renal function (creatinine [Cr]/GFR) to the starting point. Urinalysis: microscope for cells, casts, and crystals; dipstick for blood and protein Sterile pyuria (particularly WBC casts) implies AIN; 10% of individuals had the triad of fever, rash, and eosinophilia. Proteinuria, hematuria, and edoema imply GN or vasculitis and are frequently accompanied with nephritic urine sediment (RBCs and RBC casts). Casts: pigmented granular/muddy brown casts—ATN; transparent hyaline casts—prerenal aetiology; WBC casts—AIN; RBC casts—GN Eosinophils in the urine: 1% or less suggest AIN (low sensitivity). If the patient is taking diuretics, use FEurea instead of FENa: FEurea = [(Uurea PCr) / (PBUN UCr)] 100; FEurea 35% suggests prerenal aetiology. Urine electrolytes in an oliguric condition. FENa = [(UNa PCr) / (PNa UCr)] 100. Consider arterial or venous blood gas (ABG/VBG), electrolytes (including Ca/Mg/P), CBC, BUN, SCr, and electrolytes. BUN/Cr ratio is not a good indicator of prerenal azotemia versus AKI. Increased potassium, phosphate, magnesium, and uric acid are common lab abnormalities in AKI. Haemoglobin, sodium, and calcium levels fell. For accurate drug administration, determine the creatinine clearance (CrCl). Picture this: - Renal ultrasound (US): first line test that determines kidney size, hydronephrosis, and nephrolithiasis while ruling out postrenal causes. - Renal Doppler-flow US: depends on the operator; checks for renal artery stenosis/thrombosis - Kidney, ureter, bladder (KUB) abdominal x-ray: detects calcification, renal calculi, and kidney size; novel biomarkers being studied include urinary IL-18, neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), plasma cystatin C, TIMP-2, and IGFBP7 (4).[C] Tests in the Future & Special Considerations Take into account immunologic testing (if GN or vasculitis are suspected) as well as CK (rhabdomyolysis). Prerenal blockage treated with ultrasound is just as successful as CT in the event that first tests are negative. Noncontrast helical CT is the most accurate test for nephrolithiasis, and radionuclide renal scan assesses renal perfusion, function, and the presence of extravasation and obstructive uropathy. - MRI: T2-weighted signal with enhanced acute tubulointerstitial nephritis. Due to the danger of nephrogenic systemic fibrosis, gadolinium contrast is not recommended if GFR is less than 30 mL/min. Other/Diagnostic Procedures In order to detect bladder tumours, hydronephrosis, obstructions, and upper tract abnormalities without running the risk of contrast nephropathy, cystoscopy with retrograde pyelogram is used. Interpretation of Tests Kidney biopsy is a last choice if the patient does not react to treatment or if the diagnosis is still unclear; it is particularly helpful for evaluating intrinsic AKI with a cause that is unknown (AIN, GN, vasculitis, or rejection of a renal transplant). TREATMENT The cornerstone of treating AKI, both in prerenal and intrinsic kidney disease, is fluid resuscitation. Dialysis may be necessary in cases of severe kidney damage, particularly when the patient is oliguric. Finding the underlying cause is the most crucial step in treating AKI. UNSPECIFED MEASURES Determine and address the reasons that are pre- and postrenal. Stop using nephrotoxic medications and administer others renally. Carefully track your intake, output, and weight each day. Optimise cardiac output to keep the kidneys perfused. Improve your diet and take care of any infections. Volume overload, severe or increasing hyperkalemia, severe metabolic acidosis that is resistant to medical treatment, advanced uremic consequences (pericarditis, encephalopathy, bleeding diathesis), and pulmonary edoema are all indications for renal replacement therapy (RRT). First Line: MEDICATION Prevent fluid overload and repair electrolyte abnormalities, especially hyperkalemia, and find and treat the underlying cause. A monitored fluid challenge might be beneficial if the patient is oliguric and not volume-loaded. Furosemide can be used (judiciously) to treat hyperkalemia and/or volume overload but is ineffective for preventing and treating AKI. Furosemide stress testing may be used to predict mortality, the requirement for RRT, and the likelihood of AKI progression. Dopamine, natriuretic peptides, insulin-like growth factor, and thyroxine do not help treat AKI, and the dopamine agonist fenoldopam has mixed results in terms of reducing the risk of RRT and death in AKI; it is not now advised. Give IV calcium gluconate, isotonic sodium bicarbonate (only if acidemic; avoid using hypertonic "amps" of NaHCO3), glucose with insulin, and/or high-dose nebulized albuterol (to drive K+ into cells); Kayexalate and/or furosemide (to increase K+ excretion); hemodialysis if severe or resistant For oliguric patients, fluid restriction may be necessary to prevent hyponatremia from getting worse. Effective strategies for AKI prevention include isotonic IVF, once-daily aminoglycosides, use of lipid formulations of amphotericin B, and use of iso-osmolar nonionic contrast media. Metabolic acidosis (particularly pH 7.2): Sodium bicarbonate can be given (judiciously); be aware of volume overload, hypocalcemia, and hypokalemia. Avoiding hypovolemia reduces the risk of contrast-induced AKI. Isotonic saline at 1 mL/kg/hr the morning of the procedure and continuing until the next morning, or isotonic NaHCO3 at 3 ml/kg/hr before and 1 ml/kg/hr after contrast delivery, are also effective first-line treatments. Dihydropyridine calcium channel blockers may be protective in posttransplant ATN. Tamsulosin or other selective beta-blockers for bladder outlet obstruction secondary to BPH. QUESTIONS FOR REFERENCE Consider consulting a nephrologist for the following: - The possible beginning of renal replacement treatment (RRT) Consider seeking a urology consultation for obstructive nephropathy in renal transplant patients who have persistent and protracted anuria or oliguria, as well as refractory elevations in BUN and/or creatinine despite adequate fluid and/or electrolyte replacement, as well as underlying structural or functional renal disease (e.g., glomerulonephritis, SLE nephritis, cryoglobulinemia). SURGICAL AND OTHER PROCEDURE Hemodialysis catheter insertion to relieve blockage caused by retrograde ureteral catheters or percutaneous nephrostomy. ALTERNATIVE & COMPLEMENTARY MEDICINE Numerous herbal and nutritional supplements, such as aristolochic acid, ochratoxin A, Djenkol bean, impila, orellanine, and cat's claw, have the potential to be nephrotoxic. Ask the patient for a detailed history of their medications. CONSIDERATIONS FOR ADMISSION, THE INPATIENT, AND NURSING Treatment of hyperkalemia, metabolic acidosis, volume overload, and advanced uremia, which are life-threatening consequences. Give isotonic IV fluids if the patient is hypovolemic. Keep track of daily weights and fluid balance. Consider placing a urinary catheter to measure urine flow while assessing the risks of CAUTI (catheter-associated urinary tract infection). As soon as you can, remove. Prior to release, stabilise renal function and confirm treatment strategy. Dialysis, if required SUCCESSIVE RECOMMENDATIONS If there is ongoing proteinuria or renal impairment, see a nephrologist. DIET 20 to 30 kcal/kg/day in total caloric intake (1) Limit Na+ to 2 g per day (unless you're hypovolemic). If you are hyperkalemic, think about K+ restriction (2 to 3 g/day). Although there is no proof that phosphate binders are beneficial in AKI, they should be used if you are hyperphosphatemic. Avoid substances containing magnesium and aluminium. EDUCATION OF PATIENTS Keep yourself hydrated. Steer clear of nephrotoxic medications including NSAIDs and aminoglycosides. NCF (National Kidney Foundation). AKI, or acute kidney damage. Acute Kidney Injury: https://www.kidney.org/ atoz/ content PROGNOSIS Mortality rates range from 5% to 80%, depending on the underlying cause, other illnesses, and patient age. Short AKI durations are associated with high rates of recovery in both prerenal and postrenal AKI cases. Even after fully recovering from AKI, affected patients are more likely to go on to develop CKD and ESRD. Among patients who require RRT for AKI, recovery is more likely with higher baseline eGFR, AKI from ATN due to sepsis or surgery, and recovery is less likely with preexisting heart failure. Death, infection, convulsions, paralysis, peripheral edoema, heart failure (CHF), arrhythmias, uremic pericarditis, haemorrhage, hypotension, anaemia, hyperkalemia, and uremia are among the complications.
0 Comments
Leave a Reply. |
Kembara's Health SolutionsDiscovering the world of health and medicine. Archives
June 2023
Categories
All
|