This patient is experiencing hyponatremia, which is characterized by low plasma osmolality and high urine osmolality, indicating syndrome of inappropriate antidiuretic hormone secretion (SIADH). One of the most common causes of SIADH is the use of SSRIs. On the other hand, lithium, sodium bicarbonate, and corticosteroids are known to cause hypernatremia. Plasma osmolality can be calculated using the formula (2 x Na) + Glucose + Urea. In this patient, the calculated osmolality is 265 mosmol/kg, which falls within the normal range of 275-295 mosmol/kg.

Further Reading:

Syndrome of inappropriate antidiuretic hormone (SIADH) is a condition characterized by low sodium levels in the blood due to excessive secretion of antidiuretic hormone (ADH). ADH, also known as arginine vasopressin (AVP), is responsible for promoting water and sodium reabsorption in the body. SIADH occurs when there is impaired free water excretion, leading to euvolemic (normal fluid volume) hypotonic hyponatremia.

There are various causes of SIADH, including malignancies such as small cell lung cancer, stomach cancer, and prostate cancer, as well as neurological conditions like stroke, subarachnoid hemorrhage, and meningitis. Infections such as tuberculosis and pneumonia, as well as certain medications like thiazide diuretics and selective serotonin reuptake inhibitors (SSRIs), can also contribute to SIADH.

The diagnostic features of SIADH include low plasma osmolality, inappropriately elevated urine osmolality, urinary sodium levels above 30 mmol/L, and euvolemic. Symptoms of hyponatremia, which is a common consequence of SIADH, include nausea, vomiting, headache, confusion, lethargy, muscle weakness, seizures, and coma.

Management of SIADH involves correcting hyponatremia slowly to avoid complications such as central pontine myelinolysis. The underlying cause of SIADH should be treated if possible, such as discontinuing causative medications. Fluid restriction is typically recommended, with a daily limit of around 1000 ml for adults. In severe cases with neurological symptoms, intravenous hypertonic saline may be used. Medications like demeclocycline, which blocks ADH receptors, or ADH receptor antagonists like tolvaptan may also be considered.

It is important to monitor serum sodium levels closely during treatment, especially if using hypertonic saline, to prevent rapid correction that can lead to central pontine myelinolysis. Osmolality abnormalities can help determine the underlying cause of hyponatremia, with increased urine osmolality indicating dehydration or renal disease, and decreased urine osmolality suggesting SIADH or overhydration.

The intravascular volume of an infant is approximately 80 ml/kg, while in older children it is around 70 ml/kg. Dehydration itself does not lead to death, but shock can occur when there is a loss of 20 ml/kg from the intravascular space. Clinical dehydration becomes evident only after total losses greater than 25 ml/kg.

The table below summarizes the maintenance fluid requirements for well, normal children:

Bodyweight:
– First 10 kg: Daily fluid requirement of 100 ml/kg and hourly fluid requirement of 4 ml/kg.
– Second 10 kg: Daily fluid requirement of 50 ml/kg and hourly fluid requirement of 2 ml/kg.
– Subsequent kg: Daily fluid requirement of 20 ml/kg and hourly fluid requirement of 1 ml/kg.

Based on this information, the hourly maintenance fluid requirements for this child can be calculated as follows:

– First 10 kg: 4 ml/kg = 40 ml
– Second 10 kg: 2 ml/kg = 20 ml
– Subsequent kg: 1 ml/kg = 5 ml

Therefore, the total hourly maintenance fluid requirement for this child is 65 ml.

Calcium is effective in treating hyperkalaemia by counteracting the harmful effects on the heart caused by high levels of potassium. It achieves this by stabilizing the cardiac cell membrane and preventing unwanted depolarization. The onset of action is rapid, typically within 15 minutes, but the effects do not last for a long duration. Calcium is considered the first-line treatment for severe hyperkalaemia (potassium levels above 7 mmol/l) and when significant ECG abnormalities are present, such as widened QRS interval, loss of P wave, or cardiac arrhythmias. However, if the ECG only shows peaked T waves, calcium is usually not recommended.

It is important to note that calcium does not directly affect the serum potassium levels. Therefore, when administering calcium, it should be accompanied by other therapies that actively lower the serum potassium levels, such as insulin and salbutamol.

When hyperkalaemia is accompanied by hemodynamic compromise, calcium chloride is preferred over calcium gluconate. This is because calcium chloride contains approximately three times more elemental calcium than an equal volume of calcium gluconate.

Acute kidney injury (AKI), previously known as acute renal failure, is a sudden decline in kidney function. This leads to the accumulation of urea and other waste products in the body, as well as disturbances in fluid balance and electrolyte levels. AKI can occur in individuals with previously normal kidney function or those with pre-existing kidney disease, known as acute-on-chronic kidney disease. It is a relatively common condition, with approximately 15% of adults admitted to hospitals in the UK developing AKI.

AKI is categorized into three stages based on specific criteria. In stage 1, there is a rise in creatinine levels of 26 micromol/L or more within 48 hours, or a rise of 50-99% from baseline within 7 days (1.5-1.99 times the baseline). Additionally, a urine output of less than 0.5 mL/kg/hour for more than 6 hours is indicative of stage 1 AKI.

Stage 2 AKI is characterized by a creatinine rise of 100-199% from baseline within 7 days (2.0-2.99 times the baseline), or a urine output of less than 0.5 mL/kg/hour for more than 12 hours.

In stage 3 AKI, there is a creatinine rise of 200% or more from baseline within 7 days (3.0 or more times the baseline). Alternatively, a creatinine rise to 354 micromol/L or more with an acute rise of 26 micromol/L or more within 48 hours, or a rise of 50% or more within 7 days, is indicative of stage 3 AKI. Additionally, a urine output of less than 0.3 mL/kg/hour for 24 hours or anuria (no urine output) for 12 hours also falls under stage 3 AKI.

Generally speaking, if a child shows clinical signs of dehydration but does not exhibit shock, it can be assumed that they are 5% dehydrated. On the other hand, if shock is also present, it can be assumed that the child is 10% dehydrated or more. When we say 5% dehydration, it means that the body has lost 5 grams of fluid per 100 grams of body weight, which is equivalent to 50 ml of fluid per kilogram. Similarly, 10% dehydration implies a fluid loss of 100 ml per kilogram of body weight.

In the case of this child, who is 5% dehydrated, we can estimate that she has lost 50 ml of fluid per kilogram. Considering her weight of 8 kilograms, her estimated fluid loss would be 400 ml.

The clinical features of dehydration and shock are summarized below:

Dehydration (5%):
– The child appears unwell
– Normal heart rate or tachycardia
– Normal respiratory rate or tachypnea
– Normal peripheral pulses
– Normal or mildly prolonged capillary refill time (CRT)
– Normal blood pressure
– Warm extremities
– Decreased urine output
– Reduced skin turgor
– Sunken eyes
– Depressed fontanelle
– Dry mucous membranes

Clinical shock (10%):
– Pale, lethargic, mottled appearance
– Tachycardia
– Tachypnea
– Weak peripheral pulses
– Prolonged capillary refill time (CRT)
– Hypotension
– Cold extremities
– Decreased urine output
– Decreased level of consciousness

Respiratory alkalosis can be caused by hyperventilation, such as during periods of anxiety. It can also be a result of conditions like pulmonary embolism, CNS disorders (such as stroke or encephalitis), altitude, pregnancy, or the early stages of aspirin overdose.

Respiratory acidosis is often associated with chronic obstructive pulmonary disease (COPD) or life-threatening asthma. Other causes include pulmonary edema, sedative drug overdose (such as opiates or benzodiazepines), neuromuscular disease, obesity, or certain medications.

Metabolic alkalosis can occur due to vomiting, potassium depletion (often caused by diuretic usage), Cushing’s syndrome, or Conn’s syndrome.

Metabolic acidosis with a raised anion gap can be caused by conditions like lactic acidosis (which can result from hypoxemia, shock, sepsis, or infarction) or ketoacidosis (commonly seen in diabetes, starvation, or alcohol excess). Other causes include renal failure or poisoning (such as late stages of aspirin overdose, methanol, or ethylene glycol).

Metabolic acidosis with a normal anion gap can be attributed to conditions like renal tubular acidosis, diarrhea, ammonium chloride ingestion, or adrenal insufficiency.

To determine the amount of fluid that should be given to the 5-year-old child over the next 24 hours, we need to account for the following components of fluid therapy:

1. Deficit Replacement: The fluid lost due to dehydration.
2. Maintenance Fluid: The fluid needed for normal physiological needs.
3. Ongoing Losses: Any additional fluid loss (e.g., continued diarrhea or vomiting), which may need to be estimated and added if applicable.

Calculation Steps

1. Calculate the Fluid Deficit

The child is 10% dehydrated. This means that the child has lost 10% of their body weight in fluids.

• Body Weight: 20 kg
• Percentage Dehydration: 10%

Fluid Deficit=Body Weight×Percentage Dehydration

Fluid Deficit=20 kg×0.10=2 kg=2 liters=2000 ml

2. Calculate the Maintenance Fluid Requirement

Use the standard maintenance fluid calculation for children (the Holliday-Segar method):

• First 10 kg: 100 ml/kg/day
• Next 10 kg: 50 ml/kg/day

For a 20 kg child:

• First 10 kg: 10 kg×100 ml/kg/day=1000 ml/day
• Next 10 kg: 10 kg×50 ml/kg/day=500 ml/day

Total maintenance fluid requirement:

Maintenance Fluid=1000 ml+500 ml=1500 ml/day

3. Subtract the Initial Fluid Bolus

An initial fluid bolus of 20 ml/kg was given to treat shock:

• Fluid Bolus Given: 20 ml/kg×20 kg=400 ml

This amount should be subtracted from the deficit to avoid overhydration:

Remaining Deficit=2000 ml−400 ml=1600 ml

4. Total Fluid Requirement for 24 Hours

The total fluid requirement for the next 24 hours is the sum of the remaining deficit and the maintenance fluid:

Total Fluid for 24 hours=Remaining Deficit+Maintenance Fluid

Total Fluid for 24 hours=1600 ml+1500 ml=3100 ml

Acute kidney injury (AKI), previously known as acute renal failure, is a sudden decline in kidney function. This leads to the accumulation of urea and other waste products in the body, as well as disturbances in fluid balance and electrolyte levels. AKI can occur in individuals with previously normal kidney function or those with pre-existing kidney disease, known as acute-on-chronic kidney disease. It is a relatively common condition, affecting approximately 15% of adults admitted to hospitals in the UK.

AKI is categorized into three stages based on specific criteria. In stage 1, there is a rise in creatinine levels of 26 micromol/L or more within 48 hours, or a rise of 50-99% from the baseline within 7 days. Additionally, a urine output of less than 0.5 mL/kg/hour for more than 6 hours is indicative of stage 1 AKI.

Stage 2 AKI is characterized by a creatinine rise of 100-199% from the baseline within 7 days, or a urine output of less than 0.5 mL/kg/hour for more than 12 hours.

The most severe stage, stage 3 AKI, is identified by a creatinine rise of 200% or more from the baseline within 7 days. It can also be diagnosed if the creatinine level reaches 354 micromol/L or more with an acute rise of 26 micromol/L or more within 48 hours, or a rise of 50% or more within 7 days. Additionally, a urine output of less than 0.3 mL/kg/hour for 24 hours or anuria (no urine production) for 12 hours is indicative of stage 3 AKI.

All individuals diagnosed with stage 5 chronic kidney disease should be given the option to choose between haemodialysis or peritoneal dialysis. Peritoneal dialysis should be prioritized as the preferred treatment for the following groups of patients: those who still have some remaining kidney function, adult patients without major additional health conditions, and children who are two years old or younger.

Acute kidney injury (AKI), previously known as acute renal failure, is a sudden decline in kidney function. This leads to the accumulation of urea and other waste products in the body, as well as disturbances in fluid balance and electrolyte levels. AKI can occur in individuals with previously normal kidney function or those with pre-existing kidney disease, known as acute-on-chronic kidney disease. It is a relatively common condition, with approximately 15% of adults admitted to hospitals in the UK developing AKI.

AKI is categorized into three stages based on specific criteria. In stage 1, there is a rise in creatinine levels of 26 micromol/L or more within 48 hours, or a rise of 50-99% from baseline within 7 days (1.5-1.99 times the baseline). Additionally, a urine output of less than 0.5 mL/kg/hour for more than 6 hours is indicative of stage 1 AKI.

Stage 2 AKI is characterized by a creatinine rise of 100-199% from baseline within 7 days (2.0-2.99 times the baseline), or a urine output of less than 0.5 mL/kg/hour for more than 12 hours.

In stage 3 AKI, there is a creatinine rise of 200% or more from baseline within 7 days (3.0 or more times the baseline). Alternatively, a creatinine rise to 354 micromol/L or more with an acute rise of 26 micromol/L or more within 48 hours, or a rise of 50% or more within 7 days, is indicative of stage 3 AKI. Additionally, a urine output of less than 0.3 mL/kg/hour for 24 hours or anuria (no urine output) for 12 hours also falls under stage 3 AKI.

Generally speaking, if a child shows clinical signs of dehydration but does not exhibit shock, it can be assumed that they are 5% dehydrated. On the other hand, if shock is also present, it can be assumed that the child is 10% dehydrated or more. When a child is 5% dehydrated, it means that their body has lost 5 grams of fluid per 100 grams of body weight, which is equivalent to 50 ml of fluid per kilogram. In the case of 10% dehydration, the body has lost 100 ml of fluid per kilogram.

For example, if a child is 10% dehydrated and weighs 30 kilograms, their estimated fluid loss would be 100 ml/kg x 30 kg = 3000 ml.

The clinical features of dehydration and shock are summarized below:

Dehydration (5%):
– The child appears unwell
– Their heart rate may be normal or increased (tachycardia)
– Their respiratory rate may be normal or increased (tachypnea)
– Peripheral pulses are normal
– Capillary refill time (CRT) is normal or slightly prolonged
– Blood pressure is normal
– Extremities feel warm
– Urine output is decreased
– Skin turgor is reduced
– Eyes may appear sunken
– The fontanelle (soft spot on the baby’s head) may be depressed
– Mucous membranes are dry

Clinical shock (10%):
– The child appears pale, lethargic, and mottled
– Heart rate is increased (tachycardia)
– Respiratory rate is increased (tachypnea)
– Peripheral pulses are weak
– Capillary refill time (CRT) is prolonged
– Blood pressure is low (hypotension)
– Extremities feel cold
– Urine output is decreased
– Level of consciousness is decreased

The intravascular volume of an infant is approximately 80 ml/kg. As children get older, their intravascular volume decreases to around 70 ml/kg. Dehydration itself does not lead to death, but it can cause shock. Shock can occur when there is a loss of 20 ml/kg from the intravascular space. Clinical dehydration, on the other hand, is only noticeable after total losses greater than 25 ml/kg.

The table below summarizes the maintenance fluid requirements for well and normal children:

Bodyweight:
– First 10 kg: Daily fluid requirement of 100 ml/kg and hourly fluid requirement of 4 ml/kg
– Second 10 kg: Daily fluid requirement of 50 ml/kg and hourly fluid requirement of 2 ml/kg
– Subsequent kg: Daily fluid requirement of 20 ml/kg and hourly fluid requirement of 1 ml/kg

For a well and normal child weighing less than 10 kg, their daily maintenance fluid requirement would be 800 ml/day.

ACE inhibitors work by inhibiting the conversion of angiotensin I to angiotensin II. As a result, the effects of angiotensin II are reduced, leading to the dilation of vascular smooth muscle and the efferent arteriole of the glomerulus. This, in turn, has several effects on renal measurements. Firstly, it causes an increase in renal plasma flow. Secondly, it leads to a decrease in filtration fraction. Lastly, it results in a decrease in glomerular filtration rate.

Acute kidney injury (AKI), previously known as acute renal failure, is a sudden decline in kidney function. This results in the accumulation of urea and other waste products in the body and disrupts the balance of fluids and electrolytes. AKI can occur in individuals with previously normal kidney function or those with pre-existing kidney disease, known as acute-on-chronic kidney disease. It is a relatively common condition, with approximately 15% of adults admitted to hospitals in the UK developing AKI.

The causes of AKI can be categorized into pre-renal, intrinsic renal, and post-renal factors. The majority of AKI cases that develop outside of healthcare settings are due to pre-renal causes, accounting for 90% of cases. These causes typically involve low blood pressure associated with conditions like sepsis and fluid depletion. Medications, particularly ACE inhibitors and NSAIDs, are also frequently implicated.

Pre-renal:
– Volume depletion (e.g., severe bleeding, excessive vomiting or diarrhea, burns)
– Oedematous states (e.g., heart failure, liver cirrhosis, nephrotic syndrome)
– Low blood pressure (e.g., cardiogenic shock, sepsis, anaphylaxis)
– Cardiovascular conditions (e.g., severe heart failure, arrhythmias)
– Renal hypoperfusion: NSAIDs, COX-2 inhibitors, ACE inhibitors or ARBs, abdominal aortic aneurysm
– Renal artery stenosis
– Hepatorenal syndrome

Intrinsic renal:
– Glomerular diseases (e.g., glomerulonephritis, thrombosis, hemolytic-uremic syndrome)
– Tubular injury: acute tubular necrosis (ATN) following prolonged lack of blood supply
– Acute interstitial nephritis due to drugs (e.g., NSAIDs), infection, or autoimmune diseases
– Vascular diseases (e.g., vasculitis, polyarteritis nodosa, thrombotic microangiopathy, cholesterol emboli, renal vein thrombosis, malignant hypertension)
– Eclampsia

Post-renal:
– Kidney stones
– Blood clot
– Papillary necrosis
– Urethral stricture
– Prostatic hypertrophy or malignancy
– Bladder tumor
– Radiation fibrosis
– Pelvic malignancy
– Retroperitoneal

Renal disease is not commonly seen as a presenting sign or symptom, but approximately a certain percentage of individuals may develop it. In the case of meningococcal septicaemia, patients usually experience acute illness along with abnormal observations and confusion. Immune thrombocytopenia (ITP) is known to cause easy bruising and nosebleeds, but it does not have the same distribution pattern as HSP and does not come with abdominal pain or joint pain. On the other hand, viral urticaria and roseola typically result in a rash that blanches.

Further Reading:

Henoch-Schonlein purpura (HSP) is a small vessel vasculitis that is mediated by IgA. It is commonly seen in children following an infection, with 90% of cases occurring in children under 10 years of age. The condition is characterized by a palpable purpuric rash, abdominal pain, gastrointestinal upset, and polyarthritis. Renal involvement occurs in approximately 50% of cases, with renal impairment typically occurring within 1 day to 1 month after the onset of other symptoms. However, renal impairment is usually mild and self-limiting, although 10% of cases may have serious renal impairment at presentation and 1% may progress to end-stage kidney failure long term. Treatment for HSP involves analgesia for arthralgia, and treatment for nephropathy is generally supportive. The prognosis for HSP is usually excellent, with the condition typically resolving fully within 4 weeks, especially in children without renal involvement. However, around 1/3rd of patients may experience relapses, which can occur for several months.

Cephalexin is a type of cephalosporin medication that is eliminated from the body through the kidneys. Cephalosporin drugs have been linked to direct harm to the kidneys and can build up in individuals with kidney problems.

The typical dosage for cephalexin is 250 mg taken four times a day. For more severe infections or infections caused by organisms that are less susceptible to the medication, the dosage may be doubled. The manufacturer recommends reducing the frequency of dosing in individuals with kidney impairment. In cases where the glomerular filtration rate (GFR) is less than 10 ml/minute, the recommended dosage is 250-500 mg taken once or twice a day, depending on the severity of the infection.

Acute kidney injury (AKI), previously known as acute renal failure, is a sudden decline in kidney function. This results in the accumulation of urea and other waste products in the body and disrupts the balance of fluids and electrolytes. AKI can occur in individuals with previously normal kidney function or those with pre-existing kidney disease, known as acute-on-chronic kidney disease. It is a relatively common condition, with approximately 15% of adults admitted to hospitals in the UK developing AKI.

The causes of AKI can be categorized into pre-renal, intrinsic renal, and post-renal factors. The majority of AKI cases that develop outside of healthcare settings are due to pre-renal causes, accounting for 90% of cases. These causes typically involve low blood pressure associated with conditions like sepsis and fluid depletion. Medications, particularly ACE inhibitors and NSAIDs, are also frequently implicated.

Pre-renal:
– Volume depletion (e.g., severe bleeding, excessive vomiting or diarrhea, burns)
– Oedematous states (e.g., heart failure, liver cirrhosis, nephrotic syndrome)
– Low blood pressure (e.g., cardiogenic shock, sepsis, anaphylaxis)
– Cardiovascular conditions (e.g., severe heart failure, arrhythmias)
– Renal hypoperfusion: NSAIDs, COX-2 inhibitors, ACE inhibitors or ARBs, abdominal aortic aneurysm
– Renal artery stenosis
– Hepatorenal syndrome

Intrinsic renal:
– Glomerular diseases (e.g., glomerulonephritis, thrombosis, hemolytic-uremic syndrome)
– Tubular injury: acute tubular necrosis (ATN) following prolonged lack of blood supply
– Acute interstitial nephritis due to drugs (e.g., NSAIDs), infection, or autoimmune diseases
– Vascular diseases (e.g., vasculitis, polyarteritis nodosa, thrombotic microangiopathy, cholesterol emboli, renal vein thrombosis, malignant hypertension)
– Eclampsia

Post-renal:
– Kidney stones
– Blood clot
– Papillary necrosis
– Urethral stricture
– Prostatic hypertrophy or malignancy
– Bladder tumor
– Radiation fibrosis
– Pelvic malignancy
– Retroperitoneal

SIADH, also known as syndrome of inappropriate antidiuretic hormone secretion, is frequently observed in individuals diagnosed with small cell lung cancer. The condition can also be caused by malignancy, pulmonary disorders, and certain medications.

Further Reading:

Syndrome of inappropriate antidiuretic hormone (SIADH) is a condition characterized by low sodium levels in the blood due to excessive secretion of antidiuretic hormone (ADH). ADH, also known as arginine vasopressin (AVP), is responsible for promoting water and sodium reabsorption in the body. SIADH occurs when there is impaired free water excretion, leading to euvolemic (normal fluid volume) hypotonic hyponatremia.

There are various causes of SIADH, including malignancies such as small cell lung cancer, stomach cancer, and prostate cancer, as well as neurological conditions like stroke, subarachnoid hemorrhage, and meningitis. Infections such as tuberculosis and pneumonia, as well as certain medications like thiazide diuretics and selective serotonin reuptake inhibitors (SSRIs), can also contribute to SIADH.

The diagnostic features of SIADH include low plasma osmolality, inappropriately elevated urine osmolality, urinary sodium levels above 30 mmol/L, and euvolemic. Symptoms of hyponatremia, which is a common consequence of SIADH, include nausea, vomiting, headache, confusion, lethargy, muscle weakness, seizures, and coma.

Management of SIADH involves correcting hyponatremia slowly to avoid complications such as central pontine myelinolysis. The underlying cause of SIADH should be treated if possible, such as discontinuing causative medications. Fluid restriction is typically recommended, with a daily limit of around 1000 ml for adults. In severe cases with neurological symptoms, intravenous hypertonic saline may be used. Medications like demeclocycline, which blocks ADH receptors, or ADH receptor antagonists like tolvaptan may also be considered.

It is important to monitor serum sodium levels closely during treatment, especially if using hypertonic saline, to prevent rapid correction that can lead to central pontine myelinolysis. Osmolality abnormalities can help determine the underlying cause of hyponatremia, with increased urine osmolality indicating dehydration or renal disease, and decreased urine osmolality suggesting SIADH or overhydration.

Hyperkalemia is a condition where the level of potassium in the blood is higher than normal, specifically greater than 5.5 mmol/l. It can be categorized as mild, moderate, or severe depending on the potassium level. Mild hyperkalemia is when the potassium level is between 5.5-5.9 mmol/l, moderate hyperkalemia is between 6.0-6.4 mmol/l, and severe hyperkalemia is above 6.5 mmol/l. The most common cause of hyperkalemia is renal failure, which can be acute or chronic. Other causes include acidosis, adrenal insufficiency, cell lysis, and excessive potassium intake.

In the treatment of hyperkalemia, calcium plays a crucial role. It works by counteracting the harmful effects of high potassium levels on the heart by stabilizing the cardiac cell membrane. Calcium acts quickly, with its effects seen within 15 minutes, but its effects are relatively short-lived. It is considered a first-line treatment for arrhythmias and significant ECG abnormalities caused by hyperkalemia. However, it is rare to see arrhythmias occur at potassium levels below 7.5 mmol/l.

It’s important to note that calcium does not lower the serum level of potassium. Therefore, when administering calcium, other therapies that actually help lower potassium levels, such as insulin and salbutamol, should also be used. Insulin and salbutamol are effective in reducing serum potassium levels.

When choosing between calcium chloride and calcium gluconate, calcium chloride is preferred when hyperkalemia is accompanied by hemodynamic compromise. This is because calcium chloride contains three times more elemental calcium than an equal volume of calcium gluconate.

Hyperkalaemia can be identified by certain signs, such as muscle weakness, cramps, and delayed deep tendon reflexes. Additionally, there are neurological signs that may be present, including flaccid paralysis, twitching, peripheral paresthesia, weakness, and hypo-reflexia.

Further Reading:

Vasoactive drugs can be classified into three categories: inotropes, vasopressors, and unclassified. Inotropes are drugs that alter the force of muscular contraction, particularly in the heart. They primarily stimulate adrenergic receptors and increase myocardial contractility. Commonly used inotropes include adrenaline, dobutamine, dopamine, isoprenaline, and ephedrine.

Vasopressors, on the other hand, increase systemic vascular resistance (SVR) by stimulating alpha-1 receptors, causing vasoconstriction. This leads to an increase in blood pressure. Commonly used vasopressors include norepinephrine, metaraminol, phenylephrine, and vasopressin.

Electrolytes, such as potassium, are essential for proper bodily function. Solutions containing potassium are often given to patients to prevent or treat hypokalemia (low potassium levels). However, administering too much potassium can lead to hyperkalemia (high potassium levels), which can cause dangerous arrhythmias. It is important to monitor potassium levels and administer it at a controlled rate to avoid complications.

Hyperkalemia can be caused by various factors, including excessive potassium intake, decreased renal excretion, endocrine disorders, certain medications, metabolic acidosis, tissue destruction, and massive blood transfusion. It can present with cardiovascular, respiratory, gastrointestinal, and neuromuscular symptoms. ECG changes, such as tall tented T-waves, prolonged PR interval, flat P-waves, widened QRS complex, and sine wave, are also characteristic of hyperkalemia.

In summary, vasoactive drugs can be categorized as inotropes, vasopressors, or unclassified. Inotropes increase myocardial contractility, while vasopressors increase systemic vascular resistance. Electrolytes, particularly potassium, are important for bodily function, but administering too much can lead to hyperkalemia. Monitoring potassium levels and ECG changes is crucial in managing hyperkalemia.

Patients typically initiate dialysis when their glomerular filtration rate (GFR) drops to 10 ml/min. However, if the patient has diabetes, dialysis may be recommended when their GFR reaches 15 ml/min. The GFR is a measure of kidney function and indicates how well the kidneys are able to filter waste products from the blood. Dialysis is a medical procedure that helps perform the function of the kidneys by removing waste and excess fluid from the body.

The usual approach to managing SIADH without neurological symptoms is to restrict fluid intake. In this case, the patient has SIADH, as evidenced by low serum osmolality due to low sodium levels. It is important to note that the patient’s urine osmolality is high despite the low serum osmolality.

Further Reading:

Syndrome of inappropriate antidiuretic hormone (SIADH) is a condition characterized by low sodium levels in the blood due to excessive secretion of antidiuretic hormone (ADH). ADH, also known as arginine vasopressin (AVP), is responsible for promoting water and sodium reabsorption in the body. SIADH occurs when there is impaired free water excretion, leading to euvolemic (normal fluid volume) hypotonic hyponatremia.

There are various causes of SIADH, including malignancies such as small cell lung cancer, stomach cancer, and prostate cancer, as well as neurological conditions like stroke, subarachnoid hemorrhage, and meningitis. Infections such as tuberculosis and pneumonia, as well as certain medications like thiazide diuretics and selective serotonin reuptake inhibitors (SSRIs), can also contribute to SIADH.

The diagnostic features of SIADH include low plasma osmolality, inappropriately elevated urine osmolality, urinary sodium levels above 30 mmol/L, and euvolemic. Symptoms of hyponatremia, which is a common consequence of SIADH, include nausea, vomiting, headache, confusion, lethargy, muscle weakness, seizures, and coma.

Management of SIADH involves correcting hyponatremia slowly to avoid complications such as central pontine myelinolysis. The underlying cause of SIADH should be treated if possible, such as discontinuing causative medications. Fluid restriction is typically recommended, with a daily limit of around 1000 ml for adults. In severe cases with neurological symptoms, intravenous hypertonic saline may be used. Medications like demeclocycline, which blocks ADH receptors, or ADH receptor antagonists like tolvaptan may also be considered.

It is important to monitor serum sodium levels closely during treatment, especially if using hypertonic saline, to prevent rapid correction that can lead to central pontine myelinolysis. Osmolality abnormalities can help determine the underlying cause of hyponatremia, with increased urine osmolality indicating dehydration or renal disease, and decreased urine osmolality suggesting SIADH or overhydration.

Hyperkalaemia, or high levels of potassium in the blood, can be caused by various factors that are not related to drug use. These include conditions such as renal failure, where the kidneys are unable to properly regulate potassium levels, and excess potassium supplementation. Other non-drug causes include Addison’s disease, a condition characterized by adrenal insufficiency, and congenital adrenal hyperplasia. Renal tubular acidosis, specifically type 4, can also lead to hyperkalaemia. Additionally, conditions like rhabdomyolysis, burns and trauma, and tumour lysis syndrome can contribute to elevated potassium levels. Acidosis, an imbalance in the body’s pH levels, is another non-drug cause of hyperkalaemia.

On the other hand, certain medications have been associated with hyperkalaemia. These include ACE inhibitors, angiotensin receptor blockers, NSAIDs, beta-blockers, digoxin, and suxamethonium. These drugs can interfere with the body’s potassium regulation mechanisms and lead to increased levels of potassium in the blood.

In contrast, there are also conditions that result in low levels of potassium, known as hypokalaemia. Bartter’s syndrome, a rare inherited defect in the ascending limb of the loop of Henle, is characterized by hypokalaemic alkalosis and normal to low blood pressure. Type 1 and 2 renal tubular acidosis are other conditions that cause hypokalaemia. On the other hand, type 4 renal tubular acidosis leads to hyperkalaemia. Gitelman’s syndrome, another rare inherited defect, affects the distal convoluted tubule of the kidney and causes a metabolic alkalosis with hypokalaemia and hypomagnesaemia.

Lastly, excessive consumption of liquorice can result in a condition called hypermineralocorticoidism, which can lead to hypokalaemia.

Bartter’s syndrome is a rare genetic defect that affects the ascending limb of the loop of Henle. This condition is characterized by low blood pressure and a hypokalemic alkalosis, which means there is a decrease in potassium levels in the blood.

Hyperkalemia, on the other hand, is defined as having a plasma potassium level greater than 5.5 mmol/L. There are various non-drug factors that can cause hyperkalemia, such as renal failure, excessive potassium supplementation, Addison’s disease (adrenal insufficiency), congenital adrenal hyperplasia, renal tubular acidosis (type 4), rhabdomyolysis, burns and trauma, and tumor lysis syndrome. Additionally, acidosis can also contribute to the development of hyperkalemia.

In addition to these non-drug causes, certain medications can also lead to hyperkalemia. These include ACE inhibitors, angiotensin receptor blockers, NSAIDs, beta-blockers, digoxin, and suxamethonium. It is important to be aware of these potential causes and to monitor potassium levels in order to prevent and manage hyperkalemia effectively.

Hyperkalaemia is a condition where the level of potassium in the blood is higher than normal, specifically greater than 5.5 mmol/l. It can be categorized as mild, moderate, or severe depending on the specific potassium levels. Mild hyperkalaemia is when the potassium level is between 5.5-5.9 mmol/l, moderate hyperkalaemia is between 6.0-6.4 mmol/l, and severe hyperkalaemia is when the potassium level exceeds 6.5 mmol/l. The most common cause of hyperkalaemia in renal failure, which can be either acute or chronic. Other causes include acidosis, adrenal insufficiency, cell lysis, and excessive potassium intake.

If the patient’s life is not immediately at risk due to an arrhythmia, the initial treatment for hyperkalaemia should involve the use of a beta-2 agonist, such as salbutamol (2.5-10 mg). Salbutamol activates cAMP, which stimulates the Na+/K+ ATPase pump. This action helps shift potassium into the intracellular compartment. The effects of salbutamol are rapid, typically occurring within 30 minutes. With the recommended dose, a decrease in the serum potassium level of approximately 1 mmol can be expected.

Hyperkalaemia is a condition characterized by a high level of potassium in the blood, specifically a plasma potassium level greater than 5.5 mmol/l. It can be further classified into three categories based on the severity of the condition. Mild hyperkalaemia refers to a potassium level ranging from 5.5-5.9 mmol/l, while moderate hyperkalaemia is defined as a potassium level between 6.0-6.4 mmol/l. Severe hyperkalaemia is indicated by a potassium level exceeding 6.5 mmol/l.

The most common cause of hyperkalaemia in renal failure, which can occur either acutely or chronically. However, there are other factors that can contribute to this condition as well. These include acidosis, adrenal insufficiency, cell lysis, and excessive potassium intake.

Overall, hyperkalaemia is a medical condition that requires attention and management, as it can have significant implications for the body’s normal functioning.

The intravascular volume of an infant is approximately 80 ml/kg, while in older children it is around 70 ml/kg. Dehydration itself does not lead to death, but shock can. Shock can occur when there is a loss of 20 ml/kg from the intravascular space, whereas clinical dehydration is only noticeable after total losses greater than 25 ml/kg.

The table below summarizes the maintenance fluid requirements for well, normal children based on their body weight:

Bodyweight: First 10 kg
Daily fluid requirement: 100 ml/kg
Hourly fluid requirement: 4 ml/kg

Bodyweight: Second 10 kg
Daily fluid requirement: 50 ml/kg
Hourly fluid requirement: 2 ml/kg

Bodyweight: Subsequent kg
Daily fluid requirement: 20 ml/kg
Hourly fluid requirement: 1 ml/kg

In general, if a child shows clinical signs of dehydration without shock, they can be assumed to be 5% dehydrated. If shock is also present, it can be assumed that they are 10% dehydrated or more. 5% dehydration means that the body has lost 5 g per 100 g body weight, which is equivalent to 50 ml/kg of fluid. Therefore, 10% dehydration implies a loss of 100 ml/kg of fluid.

In the case of this child, they are in shock and should receive a 20 ml/kg fluid bolus. Therefore, the initial volume of fluid to administer should be 20 x 8 ml = 160 ml.

The clinical features of dehydration and shock are summarized in the table below:

Dehydration (5%):
– Appears ‘unwell’
– Normal heart rate or tachycardia
– Normal respiratory rate or tachypnea
– Normal peripheral pulses
– Normal or mildly prolonged capillary refill time (CRT)
– Normal blood pressure
– Warm extremities
– Decreased urine output
– Reduced skin turgor
– Sunken eyes
– Depressed fontanelle
– Dry mucous membranes

Clinical shock (10%):
– Pale, lethargic, mottled appearance
– Tachycardia
– Tachypnea
– Weak peripheral pulses
– Prolonged capillary refill time (CRT)
– Hypotension
– Cold extremities
– Decreased urine output
– Decreased level of consciousness

Digoxin is eliminated through the kidneys, and if renal function is compromised, it can lead to elevated levels of digoxin and potential toxicity. To address this issue, it is necessary to decrease the patient’s digoxin dosage and closely monitor their digoxin levels and electrolyte levels.

Generally speaking, if a child shows clinical signs of dehydration but does not exhibit shock, it can be assumed that they are 5% dehydrated. On the other hand, if shock is also present, it can be assumed that the child is 10% dehydrated or more. When we say 5% dehydration, it means that the body has lost 5 grams per 100 grams of body weight, which is equivalent to 50 milliliters per kilogram of fluid. Similarly, 10% dehydration implies a fluid loss of 100 milliliters per kilogram of fluid.

In the case of this child, they are 10% dehydrated, which means they have lost 100 milliliters per kilogram of fluid. Considering their weight of 30 kilograms, their estimated fluid loss amounts to 100 multiplied by 30, which equals 3000 milliliters.

Since this child is also in shock, they should receive a fluid bolus of 20 milliliters per kilogram. Therefore, the initial volume of fluid to administer would be 20 multiplied by 30 milliliters, resulting in 600 milliliters.

To summarize the clinical features of dehydration and shock, please refer below:

Dehydration (5%):
– The child appears unwell
– Normal heart rate or tachycardia
– Normal respiratory rate or tachypnea
– Normal peripheral pulses
– Normal or mildly prolonged capillary refill time (CRT)
– Normal blood pressure
– Warm extremities
– Decreased urine output
– Reduced skin turgor
– Sunken eyes
– Depressed fontanelle
– Dry mucous membranes

Clinical shock (10%):
– Pale, lethargic, mottled appearance
– Tachycardia
– Tachypnea
– Weak peripheral pulses
– Prolonged capillary refill time (CRT)
– Hypotension
– Cold extremities
– Decreased urine output
– Decreased level of consciousness

Chvostek’s sign is an indication of latent tetany and is observed in individuals with hypocalcaemia. When the angle of the jaw is tapped, the facial muscles on the same side of the face will momentarily contract.

Trousseau’s sign is another indication of latent tetany seen in hypocalcaemia. To test for this sign, a blood pressure cuff is placed around the subject’s arm and inflated to 20 mmHg above systolic blood pressure. This occludes arterial blood flow to the hand for a period of 3 to 5 minutes. In the presence of hypocalcaemia, carpopedal spasm will occur, characterized by flexion at the wrist and MCP joints, extension of the IP joints, and adduction of the thumb and fingers.

Blumberg’s sign is a diagnostic tool for peritonitis. It is considered positive when rebound tenderness is felt in the abdominal wall upon slow compression and rapid release.

Froment’s sign is a test used to assess ulnar nerve palsy, specifically evaluating the action of the adductor pollicis muscle. The patient is instructed to hold a piece of paper between their thumb and index finger. The examiner then attempts to pull the paper from between the thumb and index finger. A patient with ulnar nerve palsy will struggle to maintain a grip and may compensate by flexing the flexor pollicis longus muscle to sustain the pinching effect.

Gower’s sign is observed in children with Duchenne’s muscular dystrophy. When attempting to stand up from the ground, these children will start with both hands and feet on the floor and gradually use their hands to work up their legs until they achieve an upright posture.