Renal Failure in Burn

Renal Failure in
Burn

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

Urine
reabsorption, and aldosterone
stimulated Na, K and H transport.
 Renal Failure in Burn

Urine Formation =
Filtration +Secretion –
• Glomerular Filtration:Reabsorption
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
 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 tubulo-
interstitial 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.
Non - Oliguric
Criteria Oliguric RF 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
 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 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.
 Renal Failure in Burn

(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
– Low-dose dopamine.
– Digitalis.
– Vasodilator (Hydralazine, Nitroprusside).
– β-blocker, calcium channel blocker.
– Diuretics: especially in high-voltage electrical injury.
 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:
– Clinical nutrition.
– 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.
Management) Renal Failure in Burn

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 Molecular weight (D)
Thromboxane A2 352
PAF 524
Leukotriens 600
Complement 3a 10000
Complement 5a 11200
Interleukin 1, 2 15000
Tumor necrosis factor
17000
alpha
Interleukin 6 25000
Endotoxin 100,000
 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 high-
volume 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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