acute injury new

8/8/2019 Acute Injury New

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Acute kidney injuryAcute kidney injury

IntroductionIntroduction::

Acute kidney injury (AKI), previously called acute renal failureAcute kidney injury (AKI), previously called acute renal failure

(ARF),(ARF),is a rapid loss of kidney function. Its causes are numerousis a rapid loss of kidney function. Its causes are numerous

and include: low blood volume, exposure to toxins, and prostateand include: low blood volume, exposure to toxins, and prostate

enlargement. AKI is diagnosed on the basis of clinical history, suchenlargement. AKI is diagnosed on the basis of clinical history, such

as decreased urine production, and characteristic laboratoryas decreased urine production, and characteristic laboratory

findings, such as elevated blood urea nitrogen and creatinine.findings, such as elevated blood urea nitrogen and creatinine.

Depending on its severity, AKI may lead to a number ofDepending on its severity, AKI may lead to a number of

complications, including metabolic acidosis, high potassium levels,complications, including metabolic acidosis, high potassium levels,

changes in body fluid balance, and effects to other organ systems.changes in body fluid balance, and effects to other organ systems.

Management includes supportive care, such as renal replacementManagement includes supportive care, such as renal replacement

therapy, as well as treatment of the underlying disorder.therapy, as well as treatment of the underlying disorder.

Definition :Definition :

Introduced by the Acute Kidney Injury Network (AKIN), specific criteriaIntroduced by the Acute Kidney Injury Network (AKIN), specific criteria

exist for the diagnosis of AKI:exist for the diagnosis of AKI:

1. Rapid time course (less than 48 hours)1. Rapid time course (less than 48 hours)

2. Reduction of kidney function :2. Reduction of kidney function :

Rise in serum creatinineRise in serum creatinine

Absolute increase in serum creatinine of 0.3 mg/dl (26.4 mol/l)Absolute increase in serum creatinine of 0.3 mg/dl (26.4 mol/l)

Percentage increase in serum creatinine of 50%Percentage increase in serum creatinine of 50%

Reduction in urine output, defined as


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EpidemiologyEpidemiology

Acute kidney injury is common among hospitalized patients. It affectsAcute kidney injury is common among hospitalized patients. It affects

some 3-7% of patients admitted to the hospital and approximately 25-some 3-7% of patients admitted to the hospital and approximately 25-

30% of patients in the intensive care unit.30% of patients in the intensive care unit.

..

PathophysiologyPathophysiology

The causes of AKI traditionally are divided into 3 main categories:

prerenal, intrinsic, and postrenal.

Prerenal AKI

o Volume depletion

Renal losses (diuretics, polyuria)

GI losses (vomiting, diarrhea)

Cutaneous losses (burns, Stevens-Johnson

syndrome)

Hemorrhage

Pancreatitis

o Decreased cardiac output Heart failure

Pulmonary embolus

Acute myocardial infarction

Severe valvular disease

Abdominal compartment syndrome (tense

ascites)

o Systemic vasodilation

Sepsis

Anaphylaxis Anesthetics

Drug overdose

o Afferent arteriolar vasoconstriction

Hypercalcemia

Drugs (NSAIDs, amphotericin B, calcineurin

inhibitors, norepinephrine, radiocontrast agents)

Hepatorenal syndrome

o Efferent arteriolar vasodilation ACEIs or ARBs

o Renal artery occlusion Intrinsic AKI


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o Vascular (large and small vessel)

Renal artery obstruction (thrombosis, emboli,

dissection, vasculitis)

Renal vein obstruction (thrombosis)

Microangiopathy (TTP, hemolytic uremicsyndrome [HUS], DIC, preeclampsia)

Malignant hypertension

Scleroderma renal crisis

Transplant rejection

Atheroembolic disease

o Glomerular

Antiglomerular basement membrane (GBM)

disease (Goodpasture syndrome)

Antineutrophil cytoplasmic antibody-associated glomerulonephritis (ANCA-associated GN)

(Wegener granulomatosis, Churg-Strauss syndrome,

microscopic polyangiitis)

Immune complex GN (lupus, postinfectious,

cryoglobulinemia, primary membranoproliferative

glomerulonephritis)

o Tubular

Ischemic

Cytotoxic

Heme pigment (rhabdomyolysis,

intravascular hemolysis)

Crystals (tumor lysis syndrome, seizures,

ethylene glycol poisoning, megadose vitamin C,

acyclovir, indinavir, methotrexate)

Drugs (aminoglycosides, lithium,

amphotericin B, pentamidine, cisplatin,

ifosfamide, radiocontrast agents)

o Interstitial

Drugs (penicillins, cephalosporins, NSAIDs,proton-pump inhibitors, allopurinol, rifampin,

indinavir, mesalamine, sulfonamides)

Infection (pyelonephritis, viral nephritides)

Systemic disease (Sj gren syndrome, sarcoid,

lupus, lymphoma, leukemia, tubulonephritis, uveitis)

Postrenal AKI

o Ureteric obstruction (stone disease, tumor, fibrosis,

ligation during pelvic surgery)

o Bladder neck obstruction (benign prostatichypertrophy [BPH], cancer of the prostate [CA prostate or


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prostatic CA], neurogenic bladder, tricyclic antidepressants,

ganglion blockers, bladder tumor, stone disease,

hemorrhage/clot)

o Urethral obstruction (strictures, tumor, phimosis)

o Intra-abdominal hypertension (tense ascites)o Renal vein thrombosis

Staging:Staging:

The RIFLE criteria, proposed by the Acute Dialysis Quality InitiativeThe RIFLE criteria, proposed by the Acute Dialysis Quality Initiative

(ADQI) group, aid in the staging of patients with AKI:(ADQI) group, aid in the staging of patients with AKI:

Risk:Risk: serum creatinine increased 1.5 times or urine production ofserum creatinine increased 1.5 times or urine production of4 mg/dl) OR urine output below 0.3 ml/kg for 24rise of >44) (>4 mg/dl) OR urine output below 0.3 ml/kg for 24

hourshours

Loss:Loss: persistent AKI or complete loss of kidney function for morepersistent AKI or complete loss of kidney function for more

than 4 weeksthan 4 weeks

End-stage renal diseaseEnd-stage renal disease: complete loss of kidney function for: complete loss of kidney function for

more than 3 monthsmore than 3 months

Clinical :

History

A detailed and accurate history is crucial to aid in diagnosing the type of

AKI and in determining its subsequent treatment. A detailed history and a

physical examination in combination with routine laboratory tests are

useful in making a correct diagnosis

Distinguishing AKI from chronic renal failure is important, yet making

the distinction can be difficult. A history of chronic symptoms fatigue,


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weight loss, anorexia, nocturia, and pruritus suggests chronic renal

failure.

Physical

Obtaining a thorough physical examination is extremely important whencollecting evidence about the etiology of AKI.

Skin

o Petechiae, purpura, ecchymosis, and livedo reticularis

provide clues to inflammatory and vascular causes of AK

o Infectious diseases, thrombotic thrombocytopenic

purpura (TTP), disseminated intravascular coagulation

(DIC), and embolic phenomena can produce typical

cutaneous changes. Eyes

o Evidence of uveitis may indicate interstitial nephritis

and necrotizing vasculitis.

o Ocular palsy may indicate ethylene glycol poisoning

or necrotizing vasculitis.

o Findings suggestive of severe hypertension,

atheroembolic disease, and endocarditis may be observed on

careful examination of the eyes.

Cardiovascular system

o The most important part of the physical examination is

the assessment of cardiovascular and volume status.

o The physical examination must include pulse rate and

blood pressure recordings measured in both the supine

position and the standing position; close inspection of the

jugular venous pulse; careful examination of the heart, lungs,

skin turgor, and mucous membranes; and assessment for the

presence of peripheral edema.

o In hospitalized patients, accurate daily records of fluid

intake and urine output and daily measurements of patientweight are important.

o Blood pressure recordings can be important diagnostic

tools.

o Hypovolemia leads to hypotension; however,

hypotension may not necessarily indicate hypovolemia.

o Severe congestive cardiac failure (CHF) may also

cause hypotension. Although patients with CHF may have

low blood pressure, volume expansion is present and

effective renal perfusion is poor, which can result in AKI.


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o Severe hypertension with renal failure suggests

renovascular disease, glomerulonephritis, vasculitis, or

atheroembolic disease.

Abdomen

o Abdominal examination findings can be useful to helpdetect obstruction at the bladder outlet as the cause of renal

failure, which may be due to cancer or an enlarged prostate.

o The presence of tense ascites can indicate elevated

intra-abdominal pressure that can retard renal venous return

and result in AKI.

o The presence of an epigastric bruit suggests renal

vascular hypertension, which may predispose to AKI

Take note of the following findings during the physicalTake note of the following findings during the physical

examination:examination:

oo HypotensionHypotension

oo Volume contractionVolume contraction

oo Congestive heart failureCongestive heart failure

oo Nephrotoxic drug ingestionNephrotoxic drug ingestion

oo History of trauma or unaccustomed exertionHistory of trauma or unaccustomed exertion

oo Blood loss or transfusionsBlood loss or transfusions

oo Evidence of connective tissue disorders or autoimmune diseasesEvidence of connective tissue disorders or autoimmune diseases

oo Exposure to toxic substances, such as ethyl alcohol or ethyleneExposure to toxic substances, such as ethyl alcohol or ethylene

glycolglycol

oo Exposure to mercury vapors, lead, cadmium, or other heavy metals,Exposure to mercury vapors, lead, cadmium, or other heavy metals,

which can be encountered in welders and minerswhich can be encountered in welders and miners

People with the following comorbid conditions are at a higher riskPeople with the following comorbid conditions are at a higher risk

for developing AKI:for developing AKI:

oo HypertensionHypertension

oo Congestive cardiac failureCongestive cardiac failure

oo DiabetesDiabetes

oo Multiple myelomaMultiple myeloma


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oo Chronic infectionChronic infection

oo Myeloproliferative disorderMyeloproliferative disorder

Urine output history can be useful. Oliguria generally favors AKI.Urine output history can be useful. Oliguria generally favors AKI.

Abrupt anuria suggests acute urinary obstruction, acute and severeAbrupt anuria suggests acute urinary obstruction, acute and severe

glomerulonephritis, or embolic renal artery occlusion. A graduallyglomerulonephritis, or embolic renal artery occlusion. A gradually

diminishing urine output may indicate a urethral stricture or bladderdiminishing urine output may indicate a urethral stricture or bladder

outlet obstruction due to prostate enlargement.outlet obstruction due to prostate enlargement.

Because of a decrease in functioning nephrons, even a trivialBecause of a decrease in functioning nephrons, even a trivial

nephrotoxic insult may cause AKI to be superimposed on chronic renalnephrotoxic insult may cause AKI to be superimposed on chronic renal

insufficiency.insufficiency.

Complications

Metabolic acidosis, hyperkalemia, andpulmonary edema[12] may requiremedical treatment with sodium bicarbonate, antihyperkalemic measures,

and diuretics.

Lack of improvement with fluid resuscitation, therapy-resistant

hyperkalemia, metabolic acidosis, or fluid overload may necessitate

artificial support in the form ofdialysis orhemofiltration. Depending on

the cause, a proportion of patients will never regain full renal function,

thus having end-stage renal failure requiring lifelong dialysis or a kidney

transplant.

1. Significance of the fractional excretion of urea
http://en.wikipedia.org/wiki/Metabolic_acidosishttp://en.wikipedia.org/wiki/Hyperkalemiahttp://en.wikipedia.org/wiki/Pulmonary_edemahttp://en.wikipedia.org/wiki/Acute_kidney_injury#cite_note-11http://en.wikipedia.org/wiki/Acute_kidney_injury#cite_note-11http://en.wikipedia.org/wiki/Sodium_bicarbonatehttp://en.wikipedia.org/wiki/Fluid_replacementhttp://en.wikipedia.org/wiki/Renal_replacement_therapyhttp://en.wikipedia.org/wiki/Dialysishttp://en.wikipedia.org/wiki/Hemofiltrationhttp://en.wikipedia.org/wiki/End-stage_renal_failurehttp://en.wikipedia.org/wiki/Kidney_transplanthttp://en.wikipedia.org/wiki/Kidney_transplanthttp://en.wikipedia.org/wiki/Metabolic_acidosishttp://en.wikipedia.org/wiki/Hyperkalemiahttp://en.wikipedia.org/wiki/Pulmonary_edemahttp://en.wikipedia.org/wiki/Acute_kidney_injury#cite_note-11http://en.wikipedia.org/wiki/Sodium_bicarbonatehttp://en.wikipedia.org/wiki/Fluid_replacementhttp://en.wikipedia.org/wiki/Renal_replacement_therapyhttp://en.wikipedia.org/wiki/Renal_replacement_therapyhttp://en.wikipedia.org/wiki/Dialysishttp://en.wikipedia.org/wiki/Hemofiltrationhttp://en.wikipedia.org/wiki/End-stage_renal_failurehttp://en.wikipedia.org/wiki/Kidney_transplanthttp://en.wikipedia.org/wiki/Kidney_transplanthttp://en.wikipedia.org/wiki/Kidney_transplant


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Background

Fractional excretion of sodium (FENa) has been used in thediagnosis of acute renal failure (ARF) to distinguish between the

two main causes of ARF, prerenal state and acute tubular

necrosis (ATN). However, many patients with prerenal

disorders receive diuretics, which decrease sodium reabsorption

and thus increase FENa. In contrast, the fractional excretion of

urea nitrogen (FEUN) is primarily dependent on passive forces

and is therefore less influenced by diuretic therapy.

Methods

To test the hypothesis that FEUN might be more useful in

evaluating ARF, we prospectively compared FEUN with FENa

during 102 episodes of ARF due to either prerenal azotemia orATN.

Results

Patients were divided into three groups: those with prerenal

azotemia (N = 50), those with prerenal azotemia treated with

diuretics (N = 27), and those with ATN (N = 25). FENa was low

only in the patients with untreated plain prerenal azotemia while

it was high in both the prerenal with diuretics and the ATN

groups. FEUN was essentially identical in the two pre-renal


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groups (27.9 2.4% vs. 24.5 2.3%), and very different from the

FEUN found in ATN (58.6 3.6%, P < 0.0001). While 92% of the

patients with prerenal azotemia had a FENa


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sonography in acute post-transplantation renal failure. If serial

ultrasound studies are available and correlation with clinical and

laboratory data and nuclear medicine studies are obtained, the

correct diagnosis may be reached without the use of invasive

procedures.

Investigations

Clinical approach to the patient with acute renal

failure

History and examination in acute renal failuregeneral points


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Treat any life threatening features firstshock,

respiratory failure, hyperkalaemia

Is this acute or chronic renal impairment?

Identify the cause of acute renal failure that warrants

specific treatment

A full drug history (current, recent, and alternative

medication) is vital and any other clues from history

Is there a prerenal cause? What is the patient's

current fluid status?

Could this be obstruction?

Is intrinsic renal disease probablewhat does urine

analysis show ?

(1) Treat any life threatening features.

Hypotension, shock and respiratory failure should be

immediately apparent when assessing the patient, and clearly

these demand urgent treatment. Hyperkalaemia is less likely to

be immediately obvious. Unless changes are evident on ECG or

cardiac monitoring, it will only become apparent when

chemistry is

(2) Is this acute or chronic renal failure?

Previous laboratory data, information from case notes or GP

may provide the answer, but in many cases such information

will not be available., hypocalcaemia, and hyperphosphataemia


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are not good indicators of chronicity. Renal ultrasonography

may show small (


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linked with AIN. Rash, fever, and arthralgia are also suggestive

of AIN. Bone pain is a feature of myeloma.

Common drug causes of acute interstitial nephritis

Antimicrobial agents

Amoxycillin,

Ampicillin

Penicillin

Ciprofloxacin

Rifampicin

Sulphonamides

Cotrimoxazole

Aciclovir

NSAIDs and salicylates

Ibuprofen

Naproxen

Indomethacin

Anticonvulsants

Phenytoin

Antiulcer agents

Cimetidine

Omeprazole


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Others

Thiazide diuretics

Furosemide

Allopurinol

Mesalazine

Constitutional symptoms may point to systemic vasculitis.

These frequently precede the acute presentation by many

months, have often been dismissed by patients and clinicians

and for example, nasal stuffiness and epistaxis as the initial

symptoms of Wegener's granulomatosis), and only come to light

during a detailed review of the history. Haemoptysis could show

a pulmonaryrenal syndrome.

In currentlyor recentlyhospitalised patients, nephrotoxic

agents such as

aminoglycosides and radiocontrast media must be rigorously

excluded. After angiography renal function tends to reach its

nadir a few days after the contrast dose. Cholesterol emboli may

occur weeks or months later.

(4) Is a prerenal cause probable?

Assessing the haemodynamic status of the patient is an essential

part of the initial assessment and correction of hypovolaemia

and hypotension may form part of the initial, lifesaving,


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management. Hypotension is usually easy to spotbut can be

relative. A systolic pressure of 110mm Hg in the hypertensive

patient whose normal value is around 160mm Hg can

compromise renal perfusion. Postural hypotension (a decrease in

systolic blood pressure of 2030mm Hg from the lying to the

upright position) and the jugular venous pressure (JVP),

measured with the patient at 45 to the horizontal, are invaluable

markers of volume status. A significant postural decrease with

the JVP not visible shows volume depletion and the need for

fluid replacement, best carried out by rapid, repeated, infusions

of small volumes (250ml), through secure venous access, with

regular clinical reassessment. Once the patient is considered

euvolaemic, replacement should be stopped or pulmonary

oedema may occur. If fluid assessment is difficult ultrasound

guided placement of an internal jugular catheter to measure

central venous pressure may be necessary. The procedure is not

without risks. These are exacerbated in patients with ARF who

may have collapsed veins, and increased risks of bleeding

because of coagulopathy and platelet dysfunction. The time

taken to perform the task must not delay fluid resuscitation.

Evidence of currentor a history suggestive of recentvolume

depletion implies a prerenal cause or ATN, and response to

treatment differentiates between the two.

(5) Could this obstruction be post renal?


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ARF is usually reversible with rapid relief of obstruction, but

the longer the delay the more the long term damage. Obstruction

should be sought by history and examination, before proceeding

to urgent ultrasonography of the urinary tract. Prostatic disease

is a common cause of ARF in men. Obstructive urinary

symptoms may be elicited, a palpable bladder or hypertrophied

prostate found on examination, and/or urethral catheterisation

may yield a significant residual volume. In women, carcinoma

of the cervix may be detectable on vaginal examination. There

may be a history of renal stone disease.

Ultrasonography is an excellent tool for detecting obstruction;

noninvasive, relatively simple, fast to perform, and portable. It

also gives information on renal size. However, it is not perfect,

and will fail to show hydronephrosis in about 5% of cases.

Encasement of the renal pelvices and ureters by malignant tissue

or retroperitoneal fibrosis may result in a failure to dilate even

when obstructed, and dilatation may not be observed if there is

an additional prerenal element (with reduced GFR),

immediately after acute obstruction (


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means of confirming the diagnosis. Occasionally a trial of

ureteric stenting or percutaneous nephrostomy is required.

(6) Is intrinsic renal disease likely?

We need to exclude renal inflammation that requires urgent

diagnosis and treatment to prevent further lossand aid

recoveryof renal function. History and examination may

provide clues (for example, vasculitic rash). Urine analysis is

important and must be performed in all patients presenting with

ARF. Haematuria or proteinuria suggest intrinsic renal disease.

Urine should be microscoped and cultured. Red cell casts are

highly suggestive of glomerulonephritis although only present in

30% of cases. If intrinsic renal disease is considered probable,

further urgent investigation is essential, as is urgent referral to a

nephrologists.

managment

Management is directed at treating any life threatening features,

attempting to decrease or reverse the decline in renal function,

and if unsuccessful providing support by renal replacement

anticipating renal recovery. Hyperkalaemia, pulmonary oedema,

and severe acidosis require immediate attention. Fluid

balance,the use of diuretics and dopamine, as well as the relief


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of obstruction are all issues in the further management of the

patient

1. Hyperkalaemia

Severe hyperkalaemia (plasma potassium ([K+]p) >6.5mmol/l)

is a medical emergency because of the risk of life threatening

cardiac arrhythmias.. As [K+]p rises, a typical pattern of ECG

changes shows: peaked/tented T waves ([K+]p>6.5mmol/l);

flattening of the P wave and prolongati); on of the QRS complex

([K+]p 78mmol/land ventricular fibrillation or asystole ([K+]p

>9mmol/l) (These changes are not always consistent, however,

and patients with a normal baseline ECG may also develop

arrhythmias. Urgent treatment of hyperkalaemia should be

started if the serum potassium is >6.5mmol/l, or if any ECG

changes are present.

An ECG from a haemodialysis patient with aserum potassium of 8.0mmol/l, showing the classic

changes of significant hyperkalaemia: tented T

waves, flattening of the P wave, and prolongation

of the QRS complex.

The treatment of hyperkalaemia can be divided into four steps


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(1)Stabilization of cardiac myocyte

Calcium antagonises the effects of hyperkalaemia, stabilising

the myocardium within a few minutes of infusion and producing

a more normal ECG trace without affecting serum potassium. It

should be given immediately if P wave or QRS changes are

present. A bolus of 1020ml of 10% calcium gluconate or

chloride is given intravenously over two to five minutes

(2) Reduction in plasma potassium concentration

Treatment with calcium is a temporising measure buying time

while measures are started to reduce the serum potassium

through increasing cellular uptake. Various options exist:

.Insulin with glucose

Insulin acts rapidly to indirectly activate the cell membrane

Na+/K+ATPase and thus increase cellular potassium uptake,

probably via activation of Na+/H+ channels and an increase in

intracellular [Na+]. The addition of glucose to the insulin bolus

is necessary to prevent hypoglycaemia. Ten units of fast acting

soluble insulin should be added to 50ml of 50% dextrose and

infused over 1020minutes. A reduction in [K+]p is seen after

2030minutes.

.2 adrenergic agonists

Salbutamol binds to 2 receptors and through cytosolic second

messengers activates the Na+/K+ATPase, thus promoting


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cellular potassium uptake. Nebulised and intravenous

salbutamol produce a similar effect to insulin, but at higher

doses than used for bronchospasm (1020mg via nebuliser, or

0.5mg intravenously). insulin and dextrose plus salbutamol may

be more effective than either treatment alone.

.Sodium bicarbonate

The infusion of sodium bicarbonate has little immediate effect

on hyperkalaemia, but may be used to correct acidosis

.Removal of potassium from the body

(Ion exchange resins )

These bind potassium in the gastrointestinal tract, in exchange

for calcium or sodium, and result in increased potassium

excretion in the stool. Calcium resonium (calcium polystyrene

sulphonate) and Resonium A (sodium polystyrene sulphate) are

the most commonly used, given at an oral dose of 15 g up to

thrity daily, together with an osmotic laxative (for example,

lactulose 10ml) to prevent constipation. They can also be given

rectally. An effect takes two to three hours.

(Haemodialysis)


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this is the definitive means by which potassium can be removed

from the body, and is indicated in refractory severe

hyperkalaemia.

(Prevention of further potassium accumulation).

This can be achieved through a low potassium diet.

(2) Pulmonary oedema

The oligoanuric patient with pulmonary oedema resulting from

fluid overload (with/without underlying cardiac disease)

represents a clinical challenge., if significant ventilatory failure

is present, this must be dealt with first, through supplementary

oxygen, noninvasive ventilation, or intubation and ventilation,

depending on the state of the patient. While these measures are

being undertaken, pharmacological treatment to offload the

decompensated heart can be startedintravenous opioids

(diamorphine 2.55mg, with care taken depending on the

degree of respiratory distress) and an intravenous infusion of

nitrate (for example, glyceryl trinitrate 50mg in 50ml 0.9%

saline, at a rate of 220ml/h keeping the systolic blood pressure

>95mm Hg)and attempts made to provoke a diuresis. Much

larger doses of diuretics are required in renal failure, for

example, furosemide 250mg in 50ml 0.9% saline over one

hour, with an effect seen within one to two hours, if at all, and

which can be repeated if effective.


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If these interventions are not successful, or if the patient is in

extremis such that they seem unlikely to prove effective, then

fluid removal by renal replacement therapy is the definitive

answer. Either haemodialysis or haemofiltration can be used,

(3) Acidosis

Severe metabolic acidosis (blood pH


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drop, JVP and/or central venous pressure (CVP) normal), care

should be taken to avoid fluid overload and a maintenance

regimen started, which takes account of renal and insensible

losses, aiming for a positive balance of 500ml/day (hourly input

= previous hour's output plus 25ml). This requires accurate

observation and record keeping by nursing staff, and regular re

assessment by the clinician.

(5) Dopamine

The use of low dose (13g/kg/min) dopamine has been

advocated to increase renal perfusion in critically ill patients.

Recent studies, including a large randomised controlled trial,

have shown it to lack efficacy on renal outcome or overall

mortality. Use of dopamine may also reduce splanchnic

perfusion, depress respiration, suppress anterior pituitary

hormone release and function, and worsen renal function in

hypovolaemic or normovolaemic patients. Its routine use in

ARF is not currently justifiable.

(6) Diuretisc

There is a theoretical rationale for the use of loop diuretics in

ARFinhibition of the Na+/K+/2Cl pump in the thick

ascending limb of the loop of Henle, with subsequent decrease

in Na+/K+ATPase activity, should reduce the oxygen

requirements of these cells, and thus their susceptibility to

ischaemic damage. There are scarce clinical data to support this,


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and recent studies have either correlated the use of diuretics with

increased mortality, or shown no benefit. It seems reasonable to

use diuretics only in adequately resuscitatedbut oliguric

patients, at a dose suitable to the degree of renal impairment

(250mg furosemide intravenously over one hour is a standard

regimen), and to stop diuretic treatment if oliguria persists.

Converting oliguric to nonoliguric renal failure may help with

fluid and electrolyte management, but does not seem to affect

eventual need for dialysis or overall mortality, and should not

delay the start of renal replacement therapy when otherwise

indicated.

(7) Relief of obstruction

It is important to relieve urinary tract obstruction promptly.

Bladder outflow obstruction can be relieved by passage of a

urethral catheterwhich should be considered in all patients

with ARF to accurately measure urine output ;referal to

urologist

(8) General measures

Patients with ARF may suffer from excessive bleeding, because

of uraemia induced platelet dysfunction and coagulopathies (for

example, sepsis associated disseminated intravascular

coagulation). Correction of coagulopathy may be necessary with

blood products and vitamin K. Renal replacement therapy

(RRT) may improve platelet function. ARF is associated with


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numerous metabolic disturbances but energy expenditure is not

increased significantly.

Associated conditions such as sepsis and burns, however, often

lead to hypercatabolic states. Carbohydrate and protein

requirements should be tailored individually and ideally

delivered via the enteral route.protiens arenot prevented to avoid

catabolism but at the same time it shoudnot be increased to

aviode urea ecacerbation and this achieved by daily protein level

of 40 gm.citrus food shoud be avoided .water isnot allowed in

the 1st 24hs as the patient is hypervolemic

Parenteral administration may be necessary in some cases..

Additional water soluble vitamins may be required, as these are

removed by RRT. There is an increased susceptibility to

infection. Good infection control practices and a low threshold

for considering an infectious aetiology for any clinical

deterioration may minimise the risk. prophylaxis against deep

venous thrombosis can avoid some of the problems of prolonged

Replacement Therapy

As a broad generalisation, patients with ARF as part of a

systemic illnessoften with failure of multiple organ systems

require intensive care unit admission, given their probable needs

for intensive monitoring, nursing and support of other organ

systems. Patients with single organ renal failure can usually be

managed on a renal ward, and nephrologists will often support


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the role of the intensivist on the intensive care unit. The severity

of the ARF will determine the urgency for nephrology referral

but this should be the same day if intrinsic renal disease is

suspected.

Guidelines for the start of RRT

It must be emphasised that the patient should be viewed as a

whole, and dialysis neither started nor withheld on the basis of a

single variable. It is common practice to start RRT at an

earlier stage in patients with multiorgan failure because of

their potential for further deterioration and the benefits that RRT

may bring

Who needs dialysis? Guidelines for the initiation of renal

replacement therapy

Severe hyperkalaemia, unresponsive to medical

therapy

Fluid overload with pulmonary oedema (in the

context of acute renal failure)

Uraemia (blood urea >3050 mmol/l)

Complications of severe uraemia: encephalopathy,

pericarditis, neuropathy/myopathy

Severe acidosis (pH


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renal insufficiency: a prospective study. Am J Med 1983.

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2. Feest T G, Round A, Hamad S. Incidence of severe acute

renal failure in adults: results of a community based study. BMJ

1993. 306481483. [PMC free article] [PubMed]

3. Thadhani R, Pascual M, Bonventre J V. Acute renal failure. N

Engl J Med 1996. 33414481460. [PubMed]

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