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Toxic Metabolic Disorders

Toxic Metabolic Disorders

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TOXIC & METABOLIC DISORDERS

Cerebral Anoxia & Anoxic Encephalopathy

✓ Cerebral Anoxia

- Cerebral metabolism is almost totally dependent on an adequate supply of oxygen & glucose

- As oxygen content of arterial blood decreases → progressive decline in cerebral function

- Higher cortical function (especially the frontal lobe functions) are first to be affected

Etiology:

1. Ischemia (cardiac arrest, massive blood loss, etc.)

2. Decreased inspiration of oxygen

3. Alveolar hypoventilation

4. Impaired ventilation-perfusion relationship

5. Alveolar capillary block

6. Anemia

7. Impaired oxygen dissociation

8. Interference with cellular utilization of oxygen

Pathology:

Decreased oxygen

↓

Gray matter is first to be affected (due to its high metabolic rate)

↓

Dies immediately

Survives for 2 – 3 days

Longer survival

↓

Brain shows acute congestions,

dilated blood vessels &

petechial hemorrhage

Neuronal loss in the basal ganglia

(globus pallidus & substantia nigra)

Development of cortical

degeneration & gliosis

- Delayed postanoxic encephalopathy → individual appears to recover & later shows progressive

neurological deterioration , characterized by diffuse demyelination

Clinical Features:

- PaO

of 50 mmHg → decreased mental acuity, impairment of visual acuity, emotional lability &

loss of fine muscle coordination

- PaO

of 40 mmHg → faulty judgment, analgesia, & marked lack of coordination

- PaO

of <32 mmHg → loss of consciousness followed by decortication, decerebration, &

respiratory arrest

- Those who survive may recover completely or partially with permanent neurological deficits

(intellectual difficulties & posthypoxic & intention myoclonus)

- Severe hypoxia → comatosed for a prolonged period of time & may develop a persistent

vegetative state

✓ Persistent vegetative state – state of severe brain damage persisting for longer than 3

months in a patient who is mute, lacks recognizable mental function, & has responses

limited to primitive postural & reflex limb movements

Diagnostic Procedures:

- The cause of the anoxia must be determined to permit appropriate therapy

1. EEG

2. MRU & CT scan – will show the presence of cerebral edema

Treatment:

1. Treat the condition contributing to the hypoxia

2. Mannitol & glycerol → for increased ICP

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3. Oxygen by mask → for patients suffering from carbon monoxide

4. L-5 hydroxytryptophan or clonazepam → posthypoxic intention myoclonus

Brain Death

- Absence of clinical brain function when the proximate cause is known & demonstrably

irreversible

Diagnostic Criteria:

Triad:

1. Coma

2. Absence of brainstem function

3. Apnea

Neurological Complications of Thyroid Dysfunction

1. Hyperthyroidism

2. Hypothyroidism

✓ Hyperthyroidism

- Condition caused by overproduction of thyroid hormone (T

& T

)

Etiology:

- Usually associated with a diffuse toxic goiter (Graves disease), an autoimmune condition

- Other causes:

o Thyroiditis

o Functioning metastatic thyroid carcinoma

o Choriocarcinoma

o Testicular tumors

o Struma ovarii

o Trophoblastic tumors

Clinical Features:

- Weight loss

- Excessive fatigue

- Nervousness

- Palpitations

- Heat intolerance

- Increased perspiration

- Diarrhea in an individual with goiter

- Tachycardia

- Fine distal tremor

- Exophthalmos with or without opthalmoplegia & pretibial myxedema are seen in Graves disease

Diagnostic Procedures:

- Levels of Triidothyronine (T

), thyroxine (T

), thyroxine-binding globuline (TBG), & thyroid-

stimulating hormone (TSH) should be evaluated

Treatment:

- Radioactive iodine therapy

- Thyroidectomy

- Propanolol (Inderal) → effective in reducing sympathetic overactivity & controlling tremor

✓ Hypothyroidism

- Condition caused by deficient production of thyroid hormone

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TOXIC & METABOLIC DISORDERS Cerebral Anoxia & Anoxic Encephalopathy ✓ Cerebral Anoxia - Cerebral metabolism is almost totally dependent on an adequate supply of oxygen & glucose - As oxygen content of arterial blood decreases → progressive decline in cerebral function - Higher cortical function (especially the frontal lobe functions) are first to be affected Etiology: 1. Ischemia (cardiac arrest, massive blood loss, etc.) 2. Decreased inspiration of oxygen 3. Alveolar hypoventilation 4. Impaired ventilation-perfusion relationship 5. Alveolar capillary block 6. Anemia 7. Impaired oxygen dissociation 8. Interference with cellular utilization of oxygen Pathology: Decreased oxygen ↓ Gray matter is first to be affected (due to its high metabolic rate) ↓ ↓ ↓ Dies immediately Survives for 2 – 3 days Longer survival ↓ ↓ ↓ Brain shows acute congestions, Neuronal loss in the basal ganglia Development of cortical dilated blood vessels & (globus pallidus & substantia nigra) degeneration & gliosis petechial hemorrhage - Delayed postanoxic encephalopathy → individual appears to recover & later shows progressive neurological deterioration , characterized by diffuse demyelination Clinical Features: - PaO2 of 50 mmHg → decreased mental acuity, impairment of visual acuity, emotional lability & loss of fine muscle coordination - PaO2 of 40 mmHg → faulty judgment, analgesia, & marked lack of coordination - PaO2 of ...
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