Renal Failure in Burn For Nursing

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Major burns are considered as a syndrome:

–Local events.

–Systemic events. (Zygotic et al. 1996).

•One of the major systemic complications of sever burns is the renal failure, but it is quite clear that acute renal failure rarely occurs when adequate resuscitation is applied.

Functions of the Kidney

•Excretion (metabolic waste products: Urea, creatine).

•Regulation (pH of blood, electrolyte e.g. Na+ ,K+).

•Endocrinal functions.

–Erythropoietin.

–Renin.

–Vitamin D.

•Metabolic functions

–Degradation of peptides such as some hormones, in fasting gluconeogenesis.

–Transformations of amino acids (glutamine to NH4, synthesis of arginine and glycine).

Renal Physiology

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Gross structure of the kidney:

–Cortex.

–Medulla.

–Pyramids.

–Renal calyxes and pelvis.

–Ureter.

The nephron:

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is the basic structural and functional unit.

1. Superficial nephrons (30%). 

2. Midcortical nephrons (60%).

3. Juxtamedullary nephrons (10%).

functions: filtration, reabsorption, secretion

The initial step is the formation of a plasma ultrafiltrate (plasma without cells or proteins) at Bowman’s space through the action of hydrostatic pressure in the glomerular capillaries.

The proximal tubules reabsorb back into the peritubular capillaries about 2/3 of the Na and water and most of the bicarbonate, glucose and amino acids filtered and the little albumin.

The medullary loop of Henle reabsorbs salts with little water making the medullary interstitium rich in solutes (hyperosmolar) and delivers a solute poor, dilute fluid to the distal tubules. Thus the loop of Henle initiates the processes of urine concentration or dilution.

The distal tubules (cortical diluting segments) continue to dilute the luminal fluid through hormone stimulated transport of NaCl (aldosterone)and of Ca salts (parathormone). In the connecting segment water reabsorption becomes prominent only when antidiuretic hormone is abundant.

The collecting ducts make the final fine adjustments in composition of the urine through antidiuretic hormone stimulated water and urea reabsorption, and aldosterone stimulated Na, K and H transport.

Urine Formation = Filtration + Secretion – Reabsorption

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•Glomerular Filtration: Filtering of blood.

•Tubular Reabsorption: Absorption of substances needed by body.

•Tubular Secretion: Secretion of substances to be eliminated from the body.

-Protons (acid/base balance)

-Potassium

-Organic Ions

Urine Concentration

To use the urine output as an indicator of renal function and the effectiveness of fluid replacement in the burn patient, it is necessary to know both its volume and its concentration (osmolality).

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Renal Blood Flow

•Renal Blood Flow (RBF) = 25% of COP.

•90% to nephron + 10% maintain kidney

•Renal Plasma Flow (RPF):

–governed by hematocrit (45% or .45)

RBF = 1200ml/min

RPF = 660 ml/min = RBF x (1 – 0.HCT)

ERPF = 600 ml/min (Effective renal plasma flow)

Glomerular Filtration Rate

GFR = volume of plasma filtered every minute

= 20% ERPF = 125 ml/min

(i.e. entire plasma 3 L à 180 L filtered per day)

Filtration depends on

–Size/ shape/ charge.

–No RBC/ WBC/ platelets.

–No proteins.

–Fluid composition otherwise identical in glomerular capillary and proximal tubule.

–Blood pressure.

Autoregulation of GFR and RBF

•Changes in renal arterial resistance to control GFR:

–Afferent and efferent arteriolar feedback.

–Myogenic autoregulation

–Juxtaglomerular apparatus.

–Monitors NaCl concentration

Monitoring of Renal Failure

•24-hr urine volume, osmolarity and contents:

–Blood urea nitrogen.

–Serum creatinine.

–Creatinine clearance.

–Total urinary protein.

–Urinary microalbumin.

–Recent tests:

•24-hr urinary nacetyl-d-glucosaminidase (NAG) activity.

•Urinary malondialdehyde (MDA).

Types of Renal Failure in Burn

A- According to Cause:

–Pre-renal or functional causes (inadequate perfusion)

–Renal causes

(tubular, glomerular, or tubulo-interstitial damage)

–Post-renal causes

(obstruction)

B- According to Time of onset:

–Acute renal failure.

•Hypovolaemia.

•Massive presence of necrotic tissues.

•Septic period of the burn + bacteraemia.

•Hypercatabolic state after prolonged and unsuccessful treatment.

•Crushing injury syndrome (in electric burns).

–Late renal failure.

•After the first week.

•A consequence of gram-negative septicaemia, and effective control of the sepsis may be followed by a dramatic restoration of renal function.

•Another possible cause is drug nephrotoxicity. (Aminoglycosides if continued for several weeks).

C- According to Clinical Picture:

1.Oliguric RF.

2.Non-oliguric RF

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Prognostic Factors

–The severity of the burns.

–The fluid resuscitation (quantity and quality).

–The criteria of renal failure such as:

•Urine volume (> 0.5 ml/min).

•Blood urea nitrogen (> 50 mg/dl).

•Serum creatinine level (> 2.0 mg/ dl).

•Proteinuria (quantity and quantity).

–The factors of age, burn surface area, day of onset of ARF, and the duration of renal replacement therapy are not significant.

Pathophysiology of ARF with burn

The renal response to thermal injury is difficult to interpret, but it is quite clear that acute renal failure rarely occurs in cases where prompt and adequate resuscitation is accomplished

•Metabolic acidosis.

•Glomerulonephritis.

•Acute tubular necrosis.

•Medullary ischemia.

•Vasoconstriction.

•Tubular obstruction.

•Interstitial edema.

Morphological Changes

With an experience of post-mortem histopathology in burns, there are two pattern of change in renal failure after burning:

(i)Distal tubular necrosis.

–Widespread distal tubular necrosis: (affecting many nephrons, commonest in children and young adults).

–Focal distal tubular necrosis: (affecting only a few nephrons, was found in some patients, mainly children).

(ii)Proximal tubular necrosis.

–Proximal tubular necrosis: was found mainly in elderly cases who had nephrosclerosis.

Prophylactic Management

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•Pre-Hospital and Emergency Room Care of Burn Patients

It is mandatory to monitor carefully ECG and K+ and water loss.

1) Fluid resuscitation

2) Reverse potassium effects in cellular membrane with calcium chloride 10% (10 ml intravenously over 10 min)

3) Transfer extracellular potassium into cells:

–glucose (250-500 m1 of Dl017cW)+insulin (5-10 U)

–sodium bicarbonate (50-100 mEq over 5-10 min)

4) Remove potassium from the body by means of diuretics, potassium exchange resins or in serious cases, haemodialvsis.

5) Care about:

–Hyperventilation to avoid respiratory alkalosis.

–Sepsis

defect in osmotic regulation (diabetes insipidus)

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A. Hypernatraemia (> 115 mEq/L):

–peripheral oedema, ascites, pleural effusion, and interstitial oedema

–This is caused by several mechanisms:

•Intracellular sodium mobilization.

•Reabsorption of cellular oedema.

•Urinary retention of sodium (­­ renin, angiotensin. And ADH).

•The use of iso-/hypertonic fluids in the resuscitation phase.

•Therapeutics is performed with hypotonic fluids low sodium content

(NaCl 0.45%, + glucose) + diuretics.

•The amount of water is given by the formula:

= 0.6 x weight (kg) x (Na+ initial/Na+ normal -1).

•Correction should be performed gradually (not more than 1.5 mEq/h) to avoid cerebral oedema.

B. Hypokalaemia(< 3.5 mEq/L):

–This is caused by several mechanisms:

•Increased K+ losses (urinary, gastric, faecal).

•The intracellular shift of K+ because of the administration of carbohydrates.

•This imbalance is also increased by coexist ¯Mg .

•Potassium deficit is given by the formula:

•= 0.4 x weight (kg) x (3.5 – K+) .

•It is fundamental to monitor the ECG and plasma K+.

C. Hypocalcaemia (< 4.5 mEq/l or < 8.5 mg/dl):

After the first 48 h and is more prevalent on day 4.

It is advised to monitor the ionized fraction (about 45% of total circulating calcium), as it is independent of pH and albumin.

D. Hypomagnesaemia (< 1.5 mEq/l):

After the first 48 h, and is most prevalent on day 3.

This may cause treatment resistant of hypokalaemia.

E. Hypophosphataemia (< 2.5 mg/dl):

After day 3 post-burn and is most prevalent on day 7.

It is considered serious if < 1 mg/dl.

Fluid Resuscitation

It should be started within the first 24h post-burn:

(1) Choice of resuscitation fluid

A. Crystalloid vs colloid (Demling’s method).

B. Parkland vs Evans & Brooke formulae.

C. Hypertonic sodium solution (Monafo’s method).

D. Modified Parkland formula.

(2) Resuscitation

A. Resuscitation in the first 24 hours.

B. Resuscitation in the second 24 hours.

(3) Monitoring resuscitation

A. Urine output (adult : 40-60 ml/h, child : 1 ml/kg body wt./h).

B. Pulmonary capillary wedge pressure.

C. Cardiac output.

D. Blood PH.

E. Systemic blood pressure.

(4) causes of resuscitation failure

a)Extremes of age.

b)Delayed resuscitation.

c)Massive burns or severe electrical injury.

d)Inhalation injury or CO poisoning.

e)Pre-existing cardiac disease, cirrhosis/alcoholism, renal failure.

(5) adjuvant to resuscitation

a.Low-dose dopamine.

b.Digitalis.

c.Vasodilator (Hydralazine, Nitroprusside).

d.β-blocker, calcium channel blocker.

e.Diuretics: especially in high-voltage electrical injury.

Management

Once the diagnosis of acute tubular necrosis has been made, it is clearly indispensable to begin immediately a therapy whose foundations are:

1.Clinical nutrition.

2.Haemodialysis and Haemofiltration.

NB: No therapy to date has been shown to improve renal outcome and diuretics may worsen pre-renal syndrome.

Management (Clinical nutrition)

•Infusion with glucose only may be associated with:

–The inhibition of lipogenesis.

–An increase in the oxydization of the glucose and of the glycogen deposit.

–An increase of the catecholamines.

–Increased consumption of O2 and increased production of CO2.

•So, the use of glucose only is not advisable in the presence of respiratory failure and in the case of patients in mechanical ventilation.

•On the other hand, the combined glucose-lipids system has many advantages:

–Less metabolic overload compared to the infusion of a single substratum.

–The supply of the essential fatty acids,

–The diminished frequency of hyperglycaemia and hepatic steatosis.

–A reduced production of CO2 and consumption of O2.

Management (Haemodialysis)
Continuous Renal Replacement Therapy (CRRT)

•The basic principle of action of CRRT is the elimination of inflammatory mediators, urea, creatinine and uraemic toxins with the maintenance of water and electrolytes balance.

•It depends on four physical principles: ultrafiltration, convection, diffusion and adsorption.

•CRRT has the capacity to eliminate inflammatory mediators, depending on the type of filter used, up to 30,000-50,000 Daltons (D).

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•Types of haemofiltration:

–Pump-driven Haemofiltration system.

–Continuous Arterio-Venous Haemofiltration (CAVH) system.

•The advantage of a Pump-driven Haemofiltration system over a Continuous Arterio-Venous Haemofiltration (CAVH) system, was related to the faster elimination of toxic mediators with a molecular weight of 800-1000 Daltons by high-volume haemofiltration.

Indications of haemodialysis or haemofiltration:

A.Renal:

•Oliguric renal failure.

•Massive myoglobulinuria (in electric burns).

B.Non-renal:

•SIRS to eliminate inflammatory mediators.

•Sepsis, septic shock.

•Refractory hyperpyrexia.

•Correction of electrolyte imbalance.

•Congestive heart failure not responding to diuretics.

•ARDS (adult respiratory distress syndrome).

•Some intoxications.

•Prevention of the tumour-lysis syndrome.

Disadvantages and complications of CRRT

–Long-term interactions between blood and the membrane with possible manifestations of material incompatibility.

–Removal of substrate by filtration (glucose, amino acids).

–Risk of haemorrhage during long-term anticoagulation.

–Loss of heat due to extracorporeal system.

–Complications associated with insertion of central venous catheter.

–High price of materials.

–Some authors have doubts about the elimination of mediators.

•Antioxidants???

Conclusion

•Acute renal failure rarely occurs in cases where adequate resuscitation is applied.

•In sever burns, a persistent renal tubular damage and inflammation in spite of recovery of general renal function after a transient acute renal dysfunction usually occurs.

•An early intensive care of burn-induced renal damage is necessary in order to prevent renal complications as well as to lower the mortality in patients with major burns.

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Posted in Nephrology, Neurology, Nursing Care Plans, Nursing Intervention

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