Renal Failure in Burn

1

• Renal Failure in Burn
• Burn Unit
• Ain Shams University
• Faculty of Medicine

2

• 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.

3
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).

4
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.

5
Renal Physiology
6
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.
7
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.
8
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.
9
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.
10
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
11
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

12
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).

13
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)

14
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.

15
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

16
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).

17
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)

18
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).

19
Types of Renal Failure in Burn

• C- According to Clinical Picture
• Oliguric RF.
• Non-oliguric RF.

20
Prognostic Factors

• The severity of the burns.
• The fluid resuscitation (quantity and quality).
• The criteria of renal failure such as
• Urine volume (gt 0.5 ml/min).
• Blood urea nitrogen (gt 50 mg/dl).
• Serum creatinine level (gt 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.

21
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.

22
Morphological Changes

• With an experience of post-mortem histopathology
  in burns, there are two pattern of change in
  renal failure after burning
• 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).
• Proximal tubular necrosis.
• Proximal tubular necrosis was found mainly in
  elderly cases who had nephrosclerosis.

23
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)

24
Prophylactic Management

• The early post-resuscitation period (between days
  and 6),
• in which we consider ?Na, ?K, ?Ca, ?Mg and ?Ph.
• A. Hypernatraemia (gt 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.

25

• B. Hypokalaemia(lt 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.

26

• C. Hypocalcaemia (lt 4.5 mEq/l or lt 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 (lt 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 (lt 2.5 mg/dl)
• After day 3 post-burn and is most prevalent on
  day 7.
• It is considered serious if lt 1 mg/dl.

27
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.

28

• (4) causes of resuscitation failure
• Extremes of age.
• Delayed resuscitation.
• Massive burns or severe electrical injury.
• Inhalation injury or CO poisoning.
• Pre-existing cardiac disease, cirrhosis/alcoholism
  , renal failure.
• (5) adjuvant to resuscitation
• Low-dose dopamine.
• Digitalis.
• Vasodilator (Hydralazine, Nitroprusside).
• ß-blocker, calcium channel blocker.
• Diuretics especially in high-voltage electrical
  injury.

29
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.

30
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.

31
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).

32
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.

33
Management

• Indications of haemodialysis or haemofiltration
• Renal
• Oliguric renal failure.
• Massive myoglobulinuria (in electric burns).
• 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.

34
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???

35
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.

36
Thank You