renal failure in burns

8/3/2019 Renal Failure in Burns

1/36

Renal Failure in Burn

Renal Failure in BurnDr. Mohamed Ahmed El Rouby

Burn Unit

Ain Shams University

Faculty of Medicine


2/36


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.


3/36


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, infasting gluconeogenesis.

Transformations of amino acids (glutamine to

NH4, synthesis of arginine and glycine).


4/36


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.


5/36


Renal Physiology


6/36


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.


7/36


Renal Physiology

The proximal tubules reabsorb

back into the peritubular

capillaries about 2/3 of the Naand water and most of the

bicarbonate, glucose and amino

acids filtered and the little

albumin.


8/36


Renal Physiology

The medullary loop of Henlereabsorbs salts with little water

making the medullary

interstitium rich in solutes

(hyperosmolar) and delivers asolute poor, dilute fluid to the

distal tubules. Thus the loop of

Henle initiates the processes of

urine concentration or dilution.


9/36


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.


10/36


Renal Physiology

The collecting ducts make the final

fine adjustments in composition ofthe urine through antidiuretic

hormone stimulated water and urea

reabsorption, and aldosterone

stimulated Na, K and H transport. Urine


11/36


Urine Formation =Filtration +Secretion Reabsorption

Glomerular Filtration: Filtering ofblood.

Tubular Reabsorption: Absorption of

substances needed by body.- Water: 99% - Urea: 50%- Sodium: 99.5%

Tubular Secretion: Secretion ofsubstances to be eliminated from the

body.

- Protons (acid/base balance)- Potassium- Organic Ions


12/36


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 itsvolumeand its concentration(osmolality).


13/36


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)

R l F il i B


14/36


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.

R l F il i B


15/36


Autoregulation of GFR and RBF

Changes in renal arterial resistance tocontrol GFR:

Afferent and efferent arteriolar feedback.

Myogenic autoregulation

Juxtaglomerular apparatus.

Monitors NaCl concentration

R l F il i B


16/36


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).

R l F il i B


17/36


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)



18/36



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 unsuccessfultreatment.

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 adramatic restoration of renal function.

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



19/36



C- 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


20/36


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.



21/36


Pathophysiology of ARF with burn

The renal response to thermal injury is difficult to interpret, but itis 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.



22/36


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.



23/36


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 resuscitation2) Reverse potassium effects in cellular membrane with calciumchloride 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



24/36


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 interstitialoedema

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 xweight (kg) x(Na+ initial/Na+ normal -1).

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

Prophylactic Management



25/36


B. Hypokalaemia(< 3.5mEq/L): This is caused by several mechanisms:

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

The intracellular shift of K+

because of theadministration of carbohydrates.

This imbalance is also increased by coexist

Mg .

Potassium deficit is given by the formula:

= 0.4 xweight (kg) x(3.5 - K+) .

It is fundamental to monitor the ECG and plasma

K+.



26/36


C. Hypocalcaemia (< 4.5 mEq/l or < 8.5mg/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 ofpH 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.



27/36


Fluid Resuscitation

It should be started within thefirst24hpost-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.



28/36


(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, renalfailure.

(5) adjuvant to resuscitationa. Low-dose dopamine.

b. Digitalis.c. Vasodilator (Hydralazine, Nitroprusside).

d. -blocker, calcium channel blocker.

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



29/36

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.



30/36

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 glycogendeposit.

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 ofrespiratory failure and in the case of patients in mechanicalventilation.

On the other hand, the combined glucose-lipids system has manyadvantages:

Less metabolic overload compared to the infusion of a singlesubstratum.

The supply of the essential fatty acids,

The diminished frequency of hyperglycaemia and hepaticsteatosis.

A reduced production of CO2 and consumption of O2.



31/36

The basic principle of action ofCRRTis the elimination ofinflammatory mediators, urea, creatinine and uraemic toxinswith 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 30,000-50,000Daltons (D).

Mediator Molecular weight (D)

Thromboxane A2 352

PAF 524

Leukotriens600

Complement 3a 10000

Complement 5a 11200

Interleukin 1, 2 15000

Tumor necrosis factoralpha

17000

Interleukin 6 25000Endotoxin 100,000

Management )Haemodialysis(

Continuous Renal Replacement Therapy (CRRT)



32/36

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 tothe faster elimination of toxic mediators with a

molecular weight of 800-1000 Daltons by high-

volume haemofiltration.



33/36

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.



34/36

Management

Disadvantages and complications of CRRT Long-term interactions between blood and the

membrane with possible manifestations of materialincompatibility.

Removal of substrate by filtration (glucose, aminoacids).

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 ofmediators.

Antioxidants???



35/36

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 renalfunction 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.



36/36

Thank You

renal failure in burns

Documents