Renal Failure in Burn :: الفشل الكلوي لدى مرضى الحروق

Renal Failure in Burn


Burn UnitAin Shams UniversityFaculty of Medicine


• 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.


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 PhysiologyGross 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 Physiology


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 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 PhysiologyThe 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 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 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. Uri

ne


Urine Formation = Filtration +Secretion –

Reabsorption• Glomerular Filtration: Filtering of blood.

• Tubular Reabsorption: Absorption of substances needed by body.- Water: 99% - Urea: 50%- Sodium: 99.5%

• 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).


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/minRPF = 660 ml/min = RBF x (1 – 0.HCT) ERPF = 600 ml/min (Effective renal plasma flow)


Glomerular Filtration RateGFR = 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.


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 BurnA- According to Cause:

– Pre-renal or functional causes (inadequate perfusion)

– Renal causes (tubular, glomerular, or tubulo-interstitial damage)

– Post-renal causes (obstruction)


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).


Types of Renal Failure in BurnC- According to Clinical Picture:

1. Oliguric RF.

2. Non-oliguric RF.

Criteria Oliguric RFNon - Oliguric

RF

UOP < 0.5 ml/min > 0.5 ml/min

U:P Osmolality >1.4:1 1:1

U:P Creatinine >50:1 <20:1

Urine Na (mEq/L) <20 >80

CCR (mL/min) 15-20 <10

BUN/Cr >20 <10


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 ChangesWith 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.


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

• Pre-Hospital and Emergency Room Care of Burn PatientsIt is mandatory to monitor carefully ECG and K+ and water loss.1) Fluid resuscitation2) 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)

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.

Prophylactic Management


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 ResuscitationIt 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) ResuscitationA. Resuscitation in the first 24 hours.B. Resuscitation in the second 24 hours.

(3) Monitoring resuscitationA. 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 failurea) 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 resuscitationa. 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.


• 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 Molecular weight (D)

Thromboxane A2 352

PAF 524

Leukotriens 600

Complement 3a 10000

Complement 5a 11200

Interleukin 1, 2 15000

Tumor necrosis factor alpha

17000

Interleukin 6 25000

Endotoxin 100,000

Management) Haemodialysis(Continuous Renal Replacement Therapy

(CRRT)


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 high-volume haemofiltration.


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.


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???


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.

• 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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Renal Failure in Burn :: الفشل الكلوي لدى مرضى الحروق

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