- Sodium imbalance
The normal range for serum sodium levels in adults and older children is 137 to 145 millimoles per litre. A person with more than 145 millimoles of sodium per litre is said to have hypernatremia. A person with less than 137 millimoles per liter is said to have hyponatremia.
George’s sodium imbalance could be as a result of lung carcinoma which he suffers from. Lung carcinoma is known to cause syndrome of inappropriate anti diuretic hormone. This syndrome results in the abnormal secretion of anti-diuretic hormone. The increase in the levels of anti-diuretic hormone results in increased retention of water by the kidneys. As a result of this, the levels of sodium present in the blood gradually decrease. Given that chemotherapeutic drugs cause vomiting and diarrhea as one of the side effects, the syndrome of inappropriate anti diuretic syndrome that George has could be the result of taking drugs for lung carcinoma.
The symptoms of sodium imbalance are: headaches, seizures, confusion, muscle cramps, nausea, loss of appetite and fatigue. In cases of low levels of hyponatremia, the severity of the symptoms is dependent on the severity of the hyponatremia. Mild hyponatremia develops gradually and may not be noticeable initially. The symptoms that are associated with mild hyponatremia include: loss of appetite, fatigue, muscle cramps and nausea. Hyponatremia becomes more serious after 24 to 48 hours resulting in symptoms such as confusion, seizures, severe and headaches and eventually a coma.
- Function of ADH and SIADH
Anti- diuretic hormone is important in the regulation of fluid homeostasis in the kidneys where it results in increased reabsorption of water therefore resulting in the dilution of blood. The primary function of the anti diuretic hormone is in the distal convoluted tubule as well as the collecting duct. After an individual takes water, it goes into circulation where it causes the dilution of the plasma. The reduction of plasma osmolality is detected by osmoreceptors in the brain and they initiate a reduction in the amount of ADH being produced. This results in decreased reabsorption of water and increased secretion of urine. The osmolality of urine decreases while that of blood is restored to its normal levels..
The syndrome of inappropriate antidiuretic hormone secretion is also referred to as the Schwartz Bartter Syndrome or Syndrome of immoderate antidiuresis. It is a condition that is characterized by excessive production of the antidiuretic hormone by the posterior pituitary gland therefore resulting in hyponatremia and excessive retention of fluids. Patients with lung carcinoma, trauma of the head, encephalitis, stroke and meningitis are likely to suffer from the condition. The reduction in the osmolality of the plasma does not trigger a reduction in the amount of ADH being produced when the individual takes water. The condition is detected by the low sodium levels during laboratory testing given that the main solute in plasma is sodium. The symptoms associated with the hyponatremia include: nausea, headaches, vomiting, seizures and in extreme cases coma.
- Serum calcium and potassium levels
The normal serum calcium levels range between 8.4 and 10.4 mEq/dl. The normal potassium calcium levels range between 3. 0 and 5 mEq/L. A condition in which the concentration of potassium ions in the blood is low is referred to as hypokalemia. George has low levels of potassium as a result of excessive loss of fluids which is due to the syndrome of inappropriate ADH secretion. Vomiting which is associated with the syndrome could be one of reasons for the loss of potassium although not much potassium is lost through vomiting. It is also possible that the diuretics that have been administered to the patient in order to stem the loss of urine may have resulted in hypokalemia.
Hypokalemia has profound effects on the components of the renal acid base regulation mechanism. Hypokalemia stimulates the reabsorption HCO3- and ammoniagenesis. It also triggers the secretion of protons by the collecting duct via the stimulation of the gastric (HKα1) and colonic (HKα2) isoforms H+ -K+ ATPase and decreasing urinary citrate excretion. Hypokalemia results in intracellular acidification therefore affecting the renal acid base homeostasis. It also inhibits the secretion of aldosterone which has an effect on acid base homeostasis. Hypokalemia in some rare cases results in respiratory acidosis.
George could be experiencing hypocalcemia as a result of the loss of calcium in urine. As the concentration of hydrogen ions present in the blood plasma decreases as a consequence of SIADH, the concentration of calcium ions that are freely ionized decreases. When blood becomes alkaline, hydrogen ions that were bound to albumin dissociate from it. The freed up albumin binds to calcium therefore resulting in a decrease in the concentration of calcium ions. With every 0.1 increase in pH, the concentration of calcium decreases by 0.05mmol/L.
- Serum and urine osmolalities
The normal values for serum osmolality are 282-295 mOsm/kg while George’s serum osmolality value is 260 mOsm/kg. This value is below the normal range. The normal values for urine osmolality range between 50 and 800 mOsm/kg while the urine osmolality value for George is 1300 mOsm/kg. This value is above the normal range. The high value of urine osmolality in George’s case indicates that the kidneys are not reabsorbing water. This is because of SIADH which leads to the excessive production of anti diuretic hormone. The production of ADH is not regulated by changes in plasma osmolality therefore leading to excessive retention of water.
- Blood gas analysis
The arterial blood gas value is 7.25; an indication that it is acidotic. The PaCO2 is above 45 mmHg which indicates that the cause of the acidosis is respiratory in case of George. Given that the patient suffers from lung carcinoma and has been a smoker for a long time, the respiratory system may have been severely compromised hence resulting in respiratory acidosis. The bicarbonate values point to another cause of acidosis apart from the respiratory cause. This is because this value exceeds the normal ranges which are between 22 and 26 mEq/L.
According to the Henderson Hasselbach equation, if the plasma (HCO3-) was below 22mEq/L, it would be consistent with respiratory acidosis. In this case however, the plasma (HCO3-) is above 26 mEq/L which indicates that the acidosis may have other origins such as metabolic origins. The most likely cause of metabolic acidosis could be the impaired excretion of acid as a result of SIADH which causes excessive reabsorption of water.
In the event of metabolic acidosis, the compensatory mechanism is as follows: the central chemoreceptors in the medulla and peripheral chemoreceptors in the carotid and aortic bodies are stimulated resulting in an increase in ventilation by the lungs. As a result of the increase in ventilation, the partial pressure of carbon dioxide reduced leading to a decrease in the concentration of the H+.
In the event of respiratory acidosis, the kidneys initiate the compensation by retaining bicarbonate ions while excreting the H+. The pH therefore rises to the normal levels and the concentration of bicarbonate ions rises above normal. Compensation by the kidneys in response to respiratory acidosis is a slow process. The after effects of compensation by the kidneys take time to be noticed.
The compensation can be assessed by analyzing the blood pH. Normal blood pH indicate that the mechanisms are working as expected.
- Interventions for SIADH
IV furosemide is a loop diuretic that increases the rate of free water excretion. It mode of action entails the inhibition of the kidney’s ability to maintain a medullary concentration gradient. This form of treatment is often reserved for acute correction of SIADH as it can aid in the prevention of vascular overfilling. The hypertonic sodium solution (3%) is initiated in order to correct the low levels of sodium present in serum. This intervention works best if it administered in intervals of 3-4 hours.
The administration of hypertonic sodium solution is dependent on the body weight of the patient. For instance, if a patient weighs 70 kg, the infusion rate ought to be 70ml/h in order to increase the concentration of sodium by 1mmol/L. it is important to monitor the concentration of sodium in the patient’s serum after administering a hypertonic sodium solution in order gauge the efficacy of the treatment. The osmolality of the urine should also be determined often.
The primary treatment of SIADH entails the restriction of water intake. The water that a patient with SIADH is advised to take is often limited to 0.8l per day. This includes the water that is present in the food. This option is advised because SIADH is characterized by intracellular and extracellular retention of water. This strategy is slow hence the results take time to be noticed. The patients that are put on this mode of treatment often report feeling thirsty and dehydrated which may later on lead to recurrence of hyponatremia. Given that it is often difficult for a patient to restrict thirst, it is often common to find patients not complying with this mode of treatment. This mode of treatment is not sufficient for the treatment of severe forms of hyponatremia but can be effective in the treatment of asymptomatic hyponatremia.
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