Dehydration

Lov/ FtAMb INTRfcE.

fOiJ^E

Figure 35 Differential diagnosis between ARF and dehydration.

decrease in cardiac function will make renal hypoperfusion secondary to decrease in cardiac output very likely (Tabic I).

Table I: PRERENAL

Diseases of Renal Artery Thrombosis Stenosis, ctc.

Dehydration

Low fluid intake Fluid Losses (diarrhea, etc.)

Fluid Redistribution

.Sepsis Burns

Decreases in Heart Function

Tamponade, etc.

Good fluid balance, norma! heart function and use of nephrotoxic drugs suggests intrinsic acute renal failure ("lable 11).

Uiblc II: INTRINSIC ACUTE RENAL FAILURE

Glomeruli Vessels Interstitiurn "Ribule (ATN)

Glomerulonephritis Vasculitis Allergic interstitial Prolonged renal nephritis ischemia

Nephrotoxic

Once we have an idea of what is happening clinically, we should proceed to order a few tests that will help us to make a final diagnosis. Always look at a fresh urine sample under the microscope and send some to the laboratory to measure die urinary |>arameters shown in Table III

TUble Hit URINE SEDIMENT

Prerenal Intrinsic Acute RenaJ Failure Postrenal _

Unremarkable Granular casts L'nremarkablc

F.piiholial ccll casts WBC casts HBC casts

URINE ELECTROLYTES

Prerenal Intrinsic Acme Renal Failure Postrenal

Acute

Chronic

Na mEq/L

< 20

> 40

< 20

> 40

FeNa%1

< 1

> 1-2

< ]

> i

Oamolal it y

>500

<300

>500

<300

Urine/plasma

creatinine

> 40

< 20

> 20

< 20

Plasma BUN/

plasma creatine'

> 20

< 20

> 20

< 2U

WBC » White blood ceils KBC! = Red Mood cells.

'FeNa is the percentage of the total iNa* filtered by glomeruli, that is ewerexed in the urine

'This ratio may be increased by high protein intake, use of steroids, (J.I. bleeding, tetracyclines and hypermetabolism.

Always obtain a renal ultrasound to rule out obstruction (posircnal acute renal failure) (Tthle IV).

Tabic IV: POST ACUTE RLNAL FAILURE

Gynecological tumors Blood clots Papillary necrosis Prostatic tumors Neurogenic bladder Ureteral obstruction (bilateral) Urethral obstruction (stricture)

A diuretic phase is usually seen after releasing the obstruction. This is secondary to a decrease in concentrating ability and to an increase in excretion of urea that usually has accumulated during the obstruction.

If we suspect that the patient has intravascular volume depletion, a fluid challenge should Lie given, e.g.. infusion of 500 ml of half normal or normal saline in one hour and watch the patient closely for an increase in urine output. The fluid challenge can be repeated but there is the risk of developing acute pulmonary edema.

Suspicion of renal artery obstruction should lead to a radioisotope renal scan.

[f renal artery stenosis is suspected because a patient develops actne renal failure after the use of either an ACE Inhibitor or on angiotensin il receptfir bl"C.ki-r a rfnal scan irtith and without captopril nay help in the diagnosis. The renal scan after captopril should show worsening tunc lion in (he kidney with the stenosis compared to the renal scan without captopril.

11 is difficult to make the diagnosis of cortical necrosis without a renal biopsy. However, we can suspect il by the history, when the patient has very tow urine output f0-50ml/day') atld when the ART persist for more rh;m 6 wieeks without continuous insult 1ft the kidneys Soniciimes one or two months after the acute event we can see a granular caldidrtion outlining the periphery of the kidneys.

We sliouk! ivoid the use of i.v. contrast in patients with acute or chronic renal failure (e.g., scrum creatinine > 1,) mg/dl).

i lowcvcr, if the patient needs the use of i.v. contrast to diagnose an acute event (e.g., cerebral hemorrhage}, we Can perform a CAT Stan with contrast knowing that it may prolong the ARK

hirst we have to save the patient and then the kidneys. It] some circumstances, in Which ATN is unlikely and obstruction has been ruled <mtn it may be necessary lo perform a renal biopsy to diagnose some of lJhe other intrinsic causes of acute renal failure (e.g., idiopathic rapid progressive glomerulonephritis, Wegener's granulomatosis, polyarteritis nodosa etc).

Transplanted kidneys can suffer acute renal failure due to any of the etiologies discussed previously and the approach to diagnosis and treatment are the same as for native kidneys. However in the different la I diagnosis we hare to adti two major situations m which the acute renal failure is directly related to Hie fact that we are dealing with a transplanted kidney. These are: acutc transplant rejection and acute cyclos porine toxicity. Sometimes it is difficult to differentiate between the two and a renal biopsy may he necessary for final diagnosis Cyclosporinc blood levels are measured routinely for dose adjustment and high levels should alert the physician lo possible cyclosporin Induced renil failure. The tTeatmcnt in this case is to decrease the cydosporine dose. Acute rejection is treated with high doses oFsietviids and/or adminisiration of other immunosuppressive drugs (e.g., monoclonal antibodies).

CHAPTER V

PROPHYLAXIS AND TREATMENT

PROPHYLAXIS

We should avoid any insuit.s lo the kidneys (e.g.. nephrotoxic drugs, iodine dye etc.) Ill high risk psiiems |c.g., dialectics, open heart surgery, multiple myeloma, dehydration, CHF, pre-existing renal failure, elderly patients, eic,}, In a high risk patient thai may go through a situation that may cause acute renal failure (e.g., i.v. contrast load), we should Cake the following precautions. The patient should he well hydratcd prior to the test, even with i.v. fluids if necessary, and mannitol may be infused prophyLacdcally grams of mannitol in 500 ml of normal saline lo be started one hour before the procedure at a rate of ]Q0 ml/hr{Fig }7)). il is ■very important that i.v. fluids be continued to avoid negative fluid balance secondary to the increased diuresis from the marmilol and the iodine-containing dye (high dose furosemide can also be used}L

This period starts an the time the kidney receives the insult and continues until intrinsic acute renal failure develops The length of this period varies from one patient to another. During this time therapeutic

Plgure 37 Mannitol inftjs»on as propfiyiaxis

TREATMENT

intervention may reverse and/or diminish the severity of the AR(* (Fig. 38). During ibis period, that may last 24 hours, we can use manniiol 25 grams in 500 ml of normal saline (n.s.) to be given in 40 minutes, or high dose furosemide (300 mg in 0,5 liter of n.s. to be given in 60 minutes; or chlorothiazide 500 mg i..v. followed by furosemidc 300 nig i.v,). It is unclear by which mechanism these measures may change the course of the ATN.

In some circumstances the patients may respond to the use of diuretics with an increased urine output, but without a significant increase in the clcarancc of toxins. This is important becausc, although the patient may still need dialysis, fluid management becomcs much easier. In patients with renal failure tin; loop diuretics (e.g., furosemidc) arc the most effective, however higher doses than normal are required (e.g., furoscmidc 200 mg every 12 hours), [t is also important to remcm brr that there are circumstances in which die response to diuretics is decreased Some patients that do not respond to high doses of oral diuretics because of decreased bowel absorption (eg , intestinal wall edema) will respond to intravenous administration.The combination of different classes of diuretics may also he helpful in increasing urine output because they block sodium reabsorption at different sites of the nephron. For example, loop diuretics block sodium reabsorption primarily in the loop of Henle. 'iTierefore, sodium can be reabsorbed dis-tally either in the distal tubule or the collecting duct, decreasing The efficacy of the loop diuretic. In this situation, adding a thiazide (dislal diuretic) or spironolactone ( aldosterone antagonist) may increase urine output. Hypoalbuminemia is another circumstance in which the diuretic response may be decreased. The majority of diuretics are bound to plasma proteins which transport tliem to the kidney where they arc secreted into the tubular lumen. If hypoalhuniincniia is ¡ireseiU, only a small amount of diuretic binds Co protein while the rest leaves the intravascular space and does not reach the kidney. This can be solved by intravenous administration of albumin previously mixed with furoscmidc. Finally, the addition of low dose dopamine (I to 3 ug/kg/mln) may potentiate the effect of diuretics.

The use of atrial natriuretic peptide is still experimental and the effect of calcium channel Mockers has not yet been established.

Special mention should he made about what has been called ticmc-pigment-associated acute renal failure. In tins siting acute renal fail-

u.re is associated wlih either myoglobinuria or hemoglobinuria due lu rJiahduni^olysis or hemolysis respectively. In this setting the use of Intravenous fluids with maxmltol and urine alkalinization has shown to provide renal protection (for instance; 1/2 normal saline with 10 j$m yf i^ianniiiil and 50 mflq of sodium bicarbonate to maintain both a urine output of 2t)0 to 300 cc/lir and a urine pH above 6.5). )f good urine output is ni>t obtained within several hours the forced diuresis should be discontinued.

During this period substitution of rrnal function is required ¡o corrcct the fluid and electrolyte imbalance-

Initiate dialysis if the patient becomes uremic.

Water BfiUtnce

Records of fluid intake and output tp maintain adequate balance and avoid fluid overload are essential. intake: I V fluids

Food and drinks

Production [>f water from catabnlisni of carbohydrate, protein and lipids (see appendix). Output; Insensible losses (respiration and perspiration) If rifie Krool

Others (vomiting, nasogastric suction, etc,) ii'ig, IDaily weights are essential sitlce it is ijripoTinni io keep iti miiid that patients with A'LN are usually in a catabolic state and, without adequate caloric intake, they lose 0.2-0.5 k^/day, even one kilogram in

Figune RFsponsp.s to m^nritsl or luraserrtiJo {Lasix) ehaiiunge.
Figure 39 Wc should nairlam adequate fluid aalarcs.

hypercatahoiic situations. Therefore, if the weight of the patienl remains the same (without good nutrition) it means that he is he coining ftuid overloaded (Hg- Good caloric intake decreases cataholism ¡ind. therefore, the production of endogenous water.

Fig ire 40 Weight increases or remains itie gams, because of fluid ovcrloac (unless theno in high c a aric inlnke).

Sodium and Chloride BaUmc&

Usually patittits 3n ATW c.\.creie constant amounts of ^^.EL regard-Less of the intake. Therefore, to avoid Na 1 and CI imbalance we have io maintain some salt intake. Excessive salt restriction should not he

Run Cyecle

prescribed. (Fig. 41). Furthermore, we should avoid an excessive Intake of free water ('water without salt).

Potassium Balance

Plasma potassium increases quite rapidly in patients with ATN. Hyperkalemia can cause cardiac arrest, therefore Jt must be ciosclv followed Potassium intake should be lower than 40-60 mEq/2-i hr; cation exchange resnis (Kayexalate) O) (fig. -12) and dialysis should be used as needed.

In paddies with severe hyperkalemia (muscle weakness anil FKG changes), temporary measures to decrease plasma potassium should be used until hemodialysis is started: Ca-+ i.v. can block the effects of K+ on the heart; glucose infusion with insulin and correction of acidosis with i.v. bicarbonate shift K+ from the extracellular to the intracellular spacc.

Calcium, Phosphate and Magnesium Balance

Hypocalcemia, hyperphosphatemia and hypermagnesemia develop in. acute renal fail tire.

<1>:1 gram of Kiyexaiatc bintis 1 raEnot pOtflMittBlfrom the G.i. secretion», inpatients wiih vomiting, KiycjaUiit tail be given enema, kiyzxalajte can be administered with or without iu% sorbitol

Can Play Too Book
figure^!5 Oftnt.'íilof hyperkalfimifi insudes d¡e1 and tíayraalalo

Hypocalcemia occurs as a consequence of decreased production of 1,25 (OH)) vitamin and skeletal resistance to parathyroid hormone. Both hyperphosphatemia and hypermagnesemia a re the rcsutt of tle-L-rciased uitmury eACretion in the presence of persistent dietary intake. Oral calcium salrs (calcium ¡;irhonate,calcium citrate or calcium acetate) and aluminum salts can he given to control the hyperphosphatemia. Decrease of both oral piiospliste and magnesium should be prescribed.

In rliahdo myolysis, both severe hyperphosphatemia and hyperkalemia cail occur due to [he release of pllosphule and potassium from the damaged muscle.

In the rhabdomyolysis recovery phase, hypercalcemia call OCCur 3S a result of calcium mobilization (previously deposited in the damaged muscle), decrease of scrum phosphate due to increase of urinary phosphate and increase of calcitriol Aggressive calcium replacement in the hypocalccmic phase in this setting can lead to severe hypercalcemia in the recovery phase.

indications for Acute Dialysis

UUN > JIKJ mg/dl and/or severe uremic symptoms K h > 7 tnEq/t

Huid overload (pulmoiiüry ndrmn)

Severe acidosis (Fig.

rigute 43 Indications tor dialysis.

Usual Complications of Hemodialysis

Hypotension

Bleeding

Arrhythmias

Disequilibrium syndrome. Usually occurs ai the end ot the first and second dialysis. The symptoms includes headache, muscle twitching, nausea, vomiting, somnolence, confusion, coma and seizures.

This syndrome is caused by brain edema secondary to a decrease in plasma osmolality that occurs during hentodiidysis, which is not followed by thc same decrease in brain cell osmolality-The more uremic the patients arc. the more likely they are to develop this syndrome (changes in blood and brain pH may also play a role ifl this syndrome).Therefore, dialysis should be performed "gently" In the first two or three days by using small diah'ZerS, low blood flows and sljurt dialysis times.

The most widely used vascular access for acute dialysis arc double lumen subclavian and femoral catheters.

Dialysis Methods

Hemodialysis. An intermittent procedure performed with high blood flows (250-300 ml/min) for 3-4 hours per day as needed Requires the use of a dialysis machine to deliver dialysis fluid at a rate of 500 ml/min This technique is based on the physical concept of diffusion. Diffusion transfer is a passive transfer of solutes across a membrane, in die absence of net solvent transfer.

Peritoneal Dialysis, Performed continuously with hourly exchanges as needed.

CAVH. (Continuous arteriovenous bemofiltration). Continuous blood (<100 ml/min) filtration through a high permeability membrane to accomplish ultrafiltration rates between 200-800 ml/br Requires continuous fluid replacement and docs not need dialysis fluid. This technique is haned on the physical principle of filtration and it can be performed continuously (twenty four hours a day, seven days a wrt-k-) Filtration is the simultaneous transfer of a solvent, with a part of the solutes it contains, across a membrane.

CAVItD. (Continuous arteriovenous hemodialysis). Continuous procedure performed with low blood flows (<100 ml/min) and peritoneal dialysis fluid as dlalysate at a rate of 17 to 300 ml/min.This technique does not require the use of a dialysis machine.

CAVHHD, (Continuous arteriovenous hemodiafiltration).This is a combination Of CAVH and CAYHD.

Complications

The most frequent. complications of ATN in Period II are: infection, myocardial infarction, Ticari failure, acute gastrointestinal bleeding, disseminated intravascular coagulation (D1C) and strokes.

Treatment for patients with G.I. bleeding is emphasized in Fig. 44. If the patient needs dialysis,low dose heparin or no heparin (with some special dialyzers) can be used.We can perform hemodialysis with the so-called

Fig-ui*a 44 Thèrapy fill* G.I. fciCcc regional heparinizatiojir ^unal hepurinlution is tïie continuous infusion of heparin in I h t. hi find coining nut (if ihi ¡ulirm, wil.li mnlimioiis infusion of protamine in the blood go'ng bach into i tit- pattene to inhibit the cflect ni" the heparin in the systemic circulai inn Infusion of citrate prcdiaiyzcr and calcium postdialyï.cr, instead of heparin and protamine, have also been used to perforin regional heparinidation. In some cases of severe G.I, bleeding T have used peritoneal dialysis which docs not require the administration of any heparin.

The patient has an increase in urine output but the urine is still of poor quality. Therefore, he may still require dialysis, though it may be easier to main tain fluid balance (Fiji.

The kidney starts to excrete toxins and copious amounts of water with them (.Tig. 46). During this period, the kidney cannot concentrate the urine and loses a lot of water with electrolytes (polvuric phase). Furthermore, the urea atid toxins arc acting as osmotic diuretics increasing even more the water and electrolyte excretion. The therapeutic measures at this point arc directed toward adequate fluid and electrolyte replacement to compensate for the excessive losses. As a rule, aim for a negative fluid balance of about 500 nil to 1000 my24 hours (Fiji. 47).This decreases the amount of fluid accumulated during the oliguric phase and avoids continuous polyuria secondary to excessive fluid intake. Patients may require i.v. fluidr* to keep up with the urine output that can he as high as 10 liters/day or even more.

PERIOD III (The Kidney liegins to Open Up)

Figjne 4e> Morc urine does npt mean better urine

PERIOD IV (The Kidney Ls Working Again!)

Figured During ttis polyuria phass liie piliant srujl-J 6c n relate negative fluid

INTAKE

outpvt

Figure'17 Aim for a negative flukl balance.

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