Renal Failure in Burn

Renal Failure in Burn Dr. Mohamed Ahmed El Rouby

Burn Unit Ain Shams University Faculty of Medicine

Renal Failure in Burn

Major burns are considered as a syndrome: Local events. Systemic events. (Zogovic 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.

Renal Failure in Burn

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 Failure in Burn

Renal Physiology
Gross structure of the kidney:
Cortex. Medulla. Pyramids. Renal calyxes and pelvis. Ureter.

The nephron:
is the basic structural and functional unit. 1. Superficial nephrons (30%). 2. Midcortical nephrons (60%). 3. Juxtamedullary nephrons (10%).

functions: filtration, reabsorption, secretion.

Renal Failure in Burn

Renal Physiology

Renal Failure in Burn

Renal Physiology

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.

Renal Failure in Burn

Renal Physiology

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.

Renal Failure in Burn

Renal Physiology
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.

Renal Failure in Burn

Renal Physiology

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.

Renal Failure in Burn

Renal Physiology

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

Renal Failure in Burn

Urine Formation = Filtration +Secretion Reabsorption

Glomerular Filtration: Filtering of blood.

Tubular Reabsorption: Absorption of substances needed by body.

- Water: 99% - Sodium: 99.5% - Urea: 50%

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

Protons (acid/base balance) Potassium Organic Ions

Renal Failure in Burn

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).

Renal Failure in Burn

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)

Renal Failure in Burn

Glomerular Filtration Rate

GFR = volume of plasma filtered every minute = 20% ERPF = 125 ml/min (i.e. entire plasma 3 L 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.

Renal Failure in Burn

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

Renal Failure in Burn

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).

Renal Failure in Burn

Types of Renal Failure in Burn A- According to Cause: Pre-renal or functional causes

(inadequate perfusion)
Renal causes

(tubular, glomerular, or tubulointerstitial damage)

Post-renal causes

(obstruction)

Renal Failure in Burn

Types of Renal Failure in Burn

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).

Renal Failure in Burn

Types of Renal Failure in Burn

C- According to Clinical Picture:

1. Oliguric RF. 2. Non-oliguric RF.
Criteria UOP U:P Osmolality Oliguric RF < 0.5 ml/min >1.4:1 Non - Oliguric RF > 0.5 ml/min 1:1

U:P Creatinine Urine Na (mEq/L) CCR (mL/min) BUN/Cr

>50:1 <20 15-20 >20

<20:1 >80 <10 <10

Renal Failure in Burn

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.

Renal Failure in Burn

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.

Renal Failure in Burn

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.

Renal Failure in Burn

Prophylactic Management
The initial resuscitation period (between 0 and 36 h), characterized by Na+ and K+.
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)

Renal Failure in Burn

Prophylactic Management
The early post-resuscitation period (between days and 6), in which we consider Na+, K+, Ca, Mg and Ph.

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.

Renal Failure in Burn

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+.

Renal Failure in Burn

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.

Renal Failure in Burn

Fluid Resuscitation
It should be started within the first 24h postburn:
(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.

Renal Failure in Burn

(4) causes of resuscitation failure

a) b) c) d) e) Extremes of age. Delayed resuscitation. Massive burns or severe electrical injury. Inhalation injury or CO poisoning. Pre-existing cardiac disease, cirrhosis/alcoholism, renal failure. Low-dose dopamine. Digitalis. Vasodilator (Hydralazine, Nitroprusside). -blocker, calcium channel blocker. Diuretics: especially in high-voltage electrical injury.

(5) adjuvant to resuscitation

a. b. c. d. e.

Renal Failure in Burn

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.

Renal Failure in Burn

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.

Renal Failure in Burn

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).
Mediator
Thromboxane A2

Molecular weight (D)

352

PAF
Leukotriens Complement 3a Complement 5a Interleukin 1, 2

524
600 10000 11200 15000 17000 25000 100,000

Tumor necrosis factor alpha

Interleukin 6 Endotoxin

Renal Failure in Burn

Management
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 highvolume haemofiltration.

Renal Failure in Burn

Management
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.

Renal Failure in Burn

Management
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???

Renal Failure in Burn

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.

Renal Failure in Burn

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