METABOLIC MEDICINE MADE SIMPLE : HYPONATREMIA : CAUSES , PATHOPHYSIOLOGY & CLINICAL FEATURES

HYPONATREMIA  : CAUSES , PATHOPHYSIOLOGY & CLINICAL FEATURES

HYPONATREMIA

DEFINITION

Hyponatremia is a low sodium concentration in the blood. 

It is generally defined as a sodium concentration of less than 135 mmol/L (135 mEq/L), with severe hyponatremia being below 120 mEq/L. 

Symptoms can be absent, mild or severe. Mild symptoms include a decreased ability to think, headaches, nausea, and poor balance.

CAUSES OF HYPONATREMIA

HYPOVOLEMIC VOLUME STATUS

Total body water is lower than normal status

Diuretics

Sodium losing Disorders

Mineralocorticoid Deficiency

Vomiting

Diarrhea

Gastroenteritis

Burns

EUVOLEMIC

Total body water is in its normal range

SIADH

Glucocorticoid Deficiency

Hypothyroidism

HYPERVOLEMIC

Total body water is more than its normal range

Cardiac Failure

Hepatic Failure

Nephrotic Syndrome

PATHOPHYSIOLOGY

Gradual and longterm lowering of sodium concentration is mich well tolerated than a rapid acute fall of sodium levels.

Patients with mild hyponatremia are usually asymptomatic ( 125 – 135 mmol/l of sodium levels.)

Patients with moderate hyponatremia ( sodium 115 – 125 mmol/l) may have nausea , lethargy ,headache and dosorientation.

Patients with severe hyponatremia ( sodium of less than 115 mmol/L) can suffer from seizures ,coma and even death

CLINICAL FEATURES OF HYPONATREMIA

Hyponatremia signs and symptoms may include:

Nausea and vomiting

Headache

Confusion

Loss of energy, drowsiness and fatigue

Restlessness and irritability

Muscle weakness, spasms or cramps

Seizures

Coma

Neurology Made Simple : Coma : Clinical Examination and Management

COMA : CLINICAL EXAMINATION AND MANAGEMENT:

CLINICAL EXAMINATION IN COMA

NEUROLOGICAL EXAM :

Pupillary size and reaction : Bilateral fixed and dilated pupils indicates severe damage and are a sign of poor prognosis.

A unilateral fixed dialted pupil indicates 3rd cranial nerve lesion commonly due to uncalherniation.

Unlateral Horner”s syndrome indicates damage to the hypothalamus or lateral medullary syndrome.

Bilateral small pupils is suggestive of opiodoverdose or pontine damage.

INVESTIGATIONS

Laboratory tests

Blood samples will be taken to check for:

Complete blood count

Electrolytes, glucose, thyroid, kidney and liver function

Carbon monoxide poisoning

Drug or alcohol overdose

A spinal tap (lumbar puncture) can check for signs of infections in the nervous system. During a spinal tap, a doctor or specialist inserts a needle into the spinal canal and collects a small amount of fluid for analysis.

Brain scans

Imaging tests help doctors pinpoint areas of brain injury. Tests may include:

Computerized tomography (CT) scan. A CT scan uses a series of X-rays to create a detailed image of the brain. A CT scan can show a brain hemorrhage, tumors, strokes and other conditions. This test is often used to diagnose and determine the cause of a coma.

Magnetic resonance imaging (MRI). An MRI uses powerful radio waves and magnets to create a detailed view of the brain. An MRI can detect brain tissue damaged by an ischemic stroke, brain hemorrhages and other conditions. MRI scans are particularly useful for examining the brainstem and deep brain structures.

Electroencephalography (EEG). An EEG measures the electrical activity inside the brain. Doctors attach small electrodes to the scalp. Doctors send a low electrical current through the electrodes. The brain's electrical impulses are then recorded. This test can determine if seizures may be the cause of a coma.

MANAGEMENT OF COMA

A coma is a medical emergency.

Doctors will first check the affected person's airway and help maintain breathing (respiration) and circulation. Doctors may give breathing assistance and High flow oxygen, blood transfusions and other supportive care.

Establish iv access and monitor Oxygen saturations.

In case of hypoglycemia , if fingerprick glucose is less than 2.5 mmol/l give 50 ml of 50 % glucose iv.

In suspected opioid toxicity ,if pupils are small and respiratory rate is low ,give naloxone 400 mcg stat and repeated to a total of 1.2 mg .

Treatment varies, depending on the cause of the coma. A procedure or medications to relieve pressure on the brain due to brain swelling may be needed.

If the coma is the result of drug overdose, doctors will give medications to treat the condition. If the coma is due to seizures, doctors will administer medications to control seizures.

Other treatments may focus on medications or therapies to address an underlying disease, such as diabetes or liver disease.

Sometimes the cause of a coma can be completely reversed and the affected person will regain normal function. But if the affected person has suffered severe brain damage, he or she may sustain permanent disabilities or may never regain consciousness. The person may enter a persistent vegetative state or become brain dead.

COMA : CLINICAL FEATURES , CAUSES , CLINICAL FEATURES AND APPROACH TO DIAGNOSIS

COMA : CLINICAL FEATURES , CAUSES , CLINICAL FEATURES AND APPROACH TO DIAGNOSIS

COMA

A coma is a prolonged state of unconsciousness. 

During a coma, a person is unresponsive to his or her environment. 

The person is alive and looks like he or she is sleeping. However, unlike in a deep sleep, the person cannot be awakened by any stimulation, including pain.

Comas can be derived by natural causes, or can be medically induced.

CLINICAL FEATURES OF COMA

Patient fails to respond normally to painful stimuli, light, or sound; lacks a normal wake-sleep cycle; and does not initiate voluntary actions.

Coma patients exhibit a complete absence of wakefulness and are unable to consciously feel, speak or move.

Clinically, a coma can be defined as the inability to consistently follow a one-step command.

 It can also be defined as a score of ≤ 8 on the Glasgow Coma Scale (GCS) lasting ≥ 6 hours. 

A coma is a medical emergency. Swift action is needed to preserve life and brain function. Doctors normally order a battery of blood tests and a brain CT scan to try to determine what's causing the coma so that proper treatment can begin.

CAUSES OF COMA

Coma can be caused by a variety of causes  including  traumatic head injury, stroke, brain tumor, drug or alcohol intoxication, or even an underlying illness, such as diabetes or an infection to  name a few.

Traumatic brain injuries. Traumatic brain injuries, often caused by traffic collisions or acts of violence, are common causes of comas.

Stroke. Reduced or interrupted blood supply to the brain (stroke), which may be caused by blocked arteries or a burst blood vessel, can result in a coma.

Opiod toxicity , Post ictal , Subrachnoid haemorrhage / SAH

Tumors. Tumors in the brain or brainstem can cause a coma.

Diabetes. In people with diabetes, blood sugar levels that become too high (hyperglycemia) or too low (hypoglycemia) can cause a coma.

Lack of oxygen. People who have been rescued from drowning or those who have been resuscitated after a heart attack may not awaken due to lack of oxygen to the brain.

Infections. Infections such as encephalitis and meningitis cause swelling (inflammation) of the brain, spinal cord or the tissues that surround the brain. Severe cases of these infections can result in brain damage or a coma.

Seizures. Ongoing seizures may lead to a coma.

Toxins. Exposure to toxins, such as carbon monoxide or lead, can cause brain damage and a coma.

Drugs and alcohol. Overdosing on drugs or alcohol can result in a coma.

CLINICAL APPROACH TO DIAGNOSIS

Because people in a coma can't express themselves, doctors must rely on physical clues and information provided by families and friends. 

Be prepared to provide information about the affected person, including:

Events leading up to the coma, such as vomiting or headaches

Details about how the affected person lost consciousness, including whether it occurred suddenly or over time

Any noticeable signs or symptoms prior to losing consciousness

The affected person's medical history, including other conditions he or she may have had in the past, such as a stroke or transient ischemic attacks

Recent changes in the affected person's health or behavior

The affected person's drug use, including prescription and over-the-counter medications as well as unapproved medications or illegal, recreational drugs

PHYSICAL EXAMINATION

In a physical exam, doctors will check the affected person's movements and reflexes, response to painful stimuli, and pupil size. 

A head to toe screen is performed looking at general condition of the patient including hygiene/ nutrition status which if inadequate can indicae alcohol or drug abuse.

Look for signs of drug abuse such as needle track marks

Doctors will observe breathing patterns to help diagnose the cause of the coma. Doctors also may check the skin for signs of any bruises due to trauma.

To determine the affected person's level of consciousness, doctors may speak loudly or press on the angle of the jaw or nail bed. Doctors will watch for signs of arousal, such as vocal noises, eyes opening or movement.

Doctors will test reflexive eye movements. These tests can help determine the cause of the coma and the location of brain damage.

Doctors also may squirt ice-cold or warm water into the affected person's ear canals and observe eye reactions.

Look for any signs of chronic liver disease which suggests Alcohol abuse.

Observe any signs of trauma and bruising on head or other parts of the body.

Observe the respiratory pattern : Cheynes stokes respiration indicates bilateral cortical damage , hyperventilation suggest Metabolic acidosis oor brainstem pathology.

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METABOLIC ACIDOSIS : INVESTIGATIONS & MANAGEMENT

METABOLIC ACIDOSIS : INVESTIGATIONS & MANAGEMENT :

INVESTIGATIONS

These tests can help diagnose acidosis. They can also determine whether the cause is a breathing problem or a metabolic problem. Tests may include:

Arterial blood gas

Basic metabolic panel, (a group of blood tests that measure your sodium and potassium levels, kidney function, and other chemicals and functions)

Blood ketones

Lactic acid test

Urine ketones

Urine pH

Other tests may be needed to determine the cause of the acidosis.

MANAGEMENT OF METABOLIC ACIDOSIS

Treatment of metabolic acidosis depends on the underlying cause, and should target reversing the main process.

When considering course of treatment, it is important to distinguish between acute versus chronic forms.

Bicarbonate therapy is generally administered In patients with severe acute acidemia (pH < 7.11), or with less severe acidemia (pH 7.1-7.2) who have severe acute kidney injury.

Bicarbonate therapy is not recommended for people with less severe acidosis (pH ≥ 7.1), unless severe acute kidney injury is present.

In the BICAR-ICU trial,bicarbonate therapy for maintaining a pH >7.3 had no overall effect on the composite outcome of all-cause mortality and the presence of at least one organ failure at day 7.

However, amongst the sub-group of patients with severe acute kidney injury, bicarbonate therapy significantly decreased the primary composite outcome, and 28-day mortality, along with the need for dialysis.

Currently, the most commonly used treatment for chronic metabolic acidosis is oral bicarbonate.

The NKF/KDOQI guidelines recommend starting treatment when serum bicarbonate levels are <22 mEq/L, in order to maintain levels ≥ 22 mEq/L.

Studies investigating the effects of oral alkali therapy demonstrated improvements in serum bicarbonate levels, resulting in a slower decline in kidney function, and reduction in proteinuria – leading to a reduction in the risk of progressing to kidney failure.

However, side effects of oral alkali therapy include gastrointestinal intolerance, worsening edema, and worsening hypertension.

Furthermore, large doses of oral alkali are required to treat chronic metabolic acidosis, and the pill burden can limit adherence.

Veverimer (TRC 101) is a promising investigational drug designed to treat metabolic acidosis by binding with the acid in the gastrointestinal tract and removing it from the body through excretion in the feces, in turn decreasing the amount of acid in the body, and increasing the level of bicarbonate in the blood.