Question

When considering your assessments, EXPLAIN HOW BURNS can affect fluid, electrolyte, and acid-base balances.

Answer 1

The burn patient has a number of complex injuries that must be taken care of: in addition. the patient's condition changes substantially during the burn disease's evolution.
The initial post-burn period is characterized by cardiopulmonary instability (caused by- significant fluid shifts between compartments) and in many cases by direct injuries to the airways. With the onset of wound inflammation. immunosuppression, and infection the physiological and metabolic parameters change from those seen initially.
Therapeutics must therefore be based on know ledge of these changes in time. It is important to realize that many of the problems are predictable and can and should be prevented before they happen.

One of the many aspects of the care of the burn patient that must be monitored is the electrolyte balance. The correct approach will be considered with regard to three periods of time in relation to the main changes in each period:

• the initial resuscitation period (between 0 and 36 h). characterized by hyponatraernia and hyperkalaemia;
• the early post-resuscitation period (between days and 6). in which we consider hypernatraemia. hypokalaemia, hypocalcaemia, hypomagnesaemia. and hypophosphataetnia:
• the inflammation-infection period (also known as the hypermetabolic period). which is most evident after the first week. when several imbalances may coexist, depending whether correction was performed

In the firsrt period in major burns. intravascular volume is lost in burned and unburned tissues: this process is due to an increase in vascular permeability, increased interstitial osmotic pressure in burn tissue. and cellular oedema. with the most significant shifts occurring in the first hours.

• Hyponatraemia is frequent, and the restoration of sodium losses in the burn tissue is therefore essential hyperkalaemia is also characteristic of this period because of the massive tissue necrosis.Hyponatraemia (Na) (< 135 mEq/L) is due to extracellular sodium depletion following changes in cellular permeability.It is fundamental that sodium replacement should be performed with resuscitation fluids (lactated Ringer's. normal saline); sometimes two ampoules of sodium lactate are added to each 1000 ml of normal saline in order to increase osmolarity volume replacement with blood and the reduction of additional sodium losses are other important factors.
• Hyperkalaemia (K+) (> 5.5 mEq/1) is mainly caused by- cell lysis and tissue necrosis. Manifestations of hyperkalaemia are more pronounced in acute hyperkalaemia, and in particular affect the cardiovascular system.

  Transfer extracellular potassium into cells with

1. glucose (250-500 m1 of Dl017cW)+insulin (5-10 U)
2. sodium bicarbonate (50-100 mEq over 5-10 min)
3. hyperventilation (consider. however. the possible complications )
4. Remove potassium from the body by means of diuretics, potassium exchange resins. or. in serious cases, haemodialysis. It is mandatory to monitor carefully ECG and K+.

In the second period..
The early post-resuscitation phase is a period of transition from the shock phase to the hypermetabolic phase, and fluid strategies should change radically with a view to restoring losses due to water evaporation.The main changes in this period are:

1. hypernatremia (Na+) (> 115 mEq/1). This is caused by intracellular sodium mobilization, reabsotption of cellular oedema, urinary retention of sodium and the use of iso-/hypertonic fluids in the resuscitation phase.Therapeutics is performed with hypotonic fluids (low sodium content, with or without glucose): NaCl 0.45% .
2. hypokalemia :- This is most prevalent in the period following the first -18 h post-burn and is characterized by K+ < 3.5 mEq/l. It may be due to increased potassium losses (urinary-, gastric. faecal) and the intracellular shift of potassium because of the administration of carbohydrates.as a treatement add 20-30 mEq/L of potassium to the hypotonic fluids in order to compensate for urinary losses and intracellular shift.
3. Hypocalcaemia (Ca2+) (< 4.5 mEq/1 or < 8.5 mg/dl). This is apparent after the first 48 h post-burn and is more prevalent on day 4, lasting until 7 weeks post-burn. This electrolyte change occurs as a result of the calcium shift between fluid compartments and increased urinary losses.'
   Clinical manifestations may affect all the organ systems, especially the cardiovascular and neuromuscular system.Intravenous calcium chloride 10% (3-5 ml) or calcium gluconate 10% (10-20 ml) for 10-15 min, followed by elemental calcium (0.3-2.0 mg/kg/h).
4. Hypomagnesimia (Mg2+) (< 1.5 mE/1). This appears also later than the first 48 h, and is most prevalent on day 3 day post-burn; this condition frequently coexists with hypocalcaemia and hypokalaemia and can cause treatment resistant hypokalaemia.The commonest cause is excessive magnesium loss. Magnesium deficiency is usually treated with magnesium sulphate solutions: in mild cases, oral or intramuscular routes can be used (10 mEq every 4-6 h), while symptomatic or severe depletion should be treated with a parenteral magnesium infusion of 48 mEq over 24 h.
5. Hypophosphataemia. This is indicated by a serum phosphate concentration below 2.5 mg/dl and is considered serious if less than 1 mg/dl. This condition appears on about day 3 post-burn and is most prevalent on day 7.

regarding the acid base imbalance can cause metabolic and respiratory acidosis, the pathophysiology is

• increased catabolism: greater than after any other form of trauma
• proportionate increase in oxygen consumption
• stress response is manifested as: persistent hyperpyrexia, tachycardia, hyperventilation, hyperglycaemia
• plasma insulin low immediately after thermal injury but is usually followed by a prolonged "insulin resistance" phase
• hypermetabolism increases with cooling, pain and sepsis: hence try to increase environmental temperature, cover burn areas with heterograft to reduce evaporative loss and give analgesia
• acidosis develops within hours after > 30% burns. Has both metabolic and respiratory components. Former due to products of heat-damaged tissues and relative hypoxia
• some evidence to suggest that stress response can be modulated and reduced if enteral feeding is started in first 24 h