STUDY - Technical - New Dacian's Medicine
Acute
Confusion and Coma (2)
Translation Draft
Let's get on with it! The reduction of wakefulness is dependent in a semi-quantitative manner on the total mass of the injured cortex or reticulated activator system (RAS) and is not represented in focus in any region of the hemispheres, except that the large, acute and unilateral damage to a hemisphere, especially the left hemisphere, may cause transient dizziness even in the absence of damage to the contralateral hemisphere or the SRA.
Hemispheric lesions, in most cases, cause coma in an indirect way when a large tumor mass in one or both hemispheres compresses the secondary upper brain stem and diencephalic SRA. This is characteristic for brain haemorrhages and rapidly expansive tumors. The degree of limitation of wakefulness is also related to the suddenness of the installation of brain dysfunction or SRA compression.
This compressive side effect led to the concept of transtentorial hernia, with progressive dysfunction of the brain stem, to explain the neurological signs of coma caused by lesions caused by supratentorial mass. Herniation refers to moving brain tissue towards mass, passing a less mobile structure like hard, and placing it in a space that it doesn't normally occupy.
The usual hernias observed postmortem are transfacial (displacement of the cingulate gir under the scythe of the brain in the anterior median line), transtentorial (median temporal lobe displaced in the tentorial opening) and foraminal (forced cerebellar tonsils in the occipital hole).
Central transtentorial hernia denoting a symmetrical downward motion of the upper diencephalus (talamic region) by the tentorial opening in the median line and is suggested by myosis and dizziness. It is considered that these changes in the brain can cause a progression of the compression of the rosral brain stem to the caudal, first of the mesencephalus, then of the bridge and finally of the bulb, leading to the sequential appearance of neurological signs corresponding to the affected level and progressive decrease in alertness.
However, many patients with supratentorial mass do not follow these stereotypical patterns, for example, an orderly progression of signs from mesencephalus to bulb is rarely observed in the case of major lesions, in which all brain functions are lost almost simultaneously.
Moreover, dizziness and stupor typically occur with moderate lateral changes in the diencephalus, when there is only minimal vertical displacement of structures near the tentoral opening and before the downward hernia is evident at TC or MRI scan.
Now you can move on to a few presentation of a few "things" about the physiopathology of come and confusion. Coma of metabolic origin is produced by interrupting the supply of energy substrate (hypoxia, ischemia, hypoglycaemia) or by altering the neurophysiological responses of neural membranes (drug or alcohol poisoning, toxic endogenous metabolites, anesthesia or epilepsy).
The same metabolic abnormalities can cause generalized neuronal dysfunction in the cortex, which diminishes all mental aspects and causes an acute confusional state. In this way, acute confusion and coma can be seen as a continuous metabolic encephalopathy.
The brain is dependent on continuous cerebral blood flow (FSC), oxygen and glucose. The brain's glucose reserves provide energy for about 2 minutes after blood flow is interrupted and consciousness is lost within 8-10 seconds.
When hypoxia is installed simultaneously with ischemia, glucose in reserves is consumed much faster. When the average FSC drops below one-third of the normal average, the EEG is diffusely slowed (typical for metabolic encephalopathy) and when it drops below about one-fifth the electrical activity of the brain ceases. If all other conditions, such as temperature and arterial oxygenation, remain normal, with an FSC lowered below about one-seventh of normal, irreversible brain damage is achieved.
The rapidity of enlargement and the duration of ischemia are also major determinants of irreversible impairment. Coma and confusion due to hyponatremia, hyperosmolarity, hypercapnia, hypercalcemia and renal or hepatic encephalopathy are associated with a variety of metabolic disorders of neurons and astrocytes.
The reversible toxic effects of these disorders on the brain are not well understood, but can, in various cases, disrupt energy reserves, change ion flows through the neural membrane and cause abnormalities in neurotransmission.
For example, increased concentrations of brain ammonia associated with hepatic coma interfere with brain energy metabolism, and the ATP-acase pump of Na+ and K+ increases the number and size of astrocytes, causes increased concentrations of potentially toxic ammonia metabolism products and produces neurotransmitter abnormalities, including possible "false" neurotransmitters, which can act competitively at the receiving site.
Ammonia and other metabolites may also bind to gamma-aminobutyric-acid receptors, leading to CNS depression through endogenous mechanisms. Moreover, these changes are not exclusively reciprocal.
The mechanism of encephalopathy in renal failure is also very little understood. Unlike ammonia, urea itself does not produce toxicity to the central nervous system (CNS). A multifactorial cause is possible, including increased permeability of the blood-brain barrier to toxic substances such as organic acids and an increase in cerebral calcium or phosphate content of cerebrospinal fluid (CRL). Osmolarity abnormalities are involved in coma and seizures caused by several systemic medical disorders, including diabetic ketoacidosis, noncetosic hyperosmolarity and hyponatremia.
The volume of water in the brain best correlates with the level of consciousness in the hyperosmolar-hyponatremic state, but there are probably other factors that play a role. Low sodium levels are associated with acute or sub acute confusion and severely reduced levels are associated with coma and seizures, depending on the rapidity with which hyponatremia develops.
Hipepappnia produces a decreased level of consciousness, proportional to the pressure of carbon dioxide in the blood and the suddenness of the onset. A correlation has been established between CRL acidosis and the severity of symptoms.
The physiology of other metabolic encephalopathy such as hypercalcemia, hypothyroidism, vitamin B12 deficiency and hypothermia are poorly understood, but should also reflect disorders in CNS biochemistry and membrane function. It turns out that the large group of CNS depressive drugs, anesthetics and some endogenous toxins produce coma through suppression of both the SRA and the cerebral cortex.
For this reason, combinations of signs of damage to the brain stem occur in the overdose of drugs and other metabolic comets, which can lead to the specific diagnosis of structural lesion of the brain stem. Although all metabolic disorders alter neuronal electrophysiology, the only main disorder of electrical brain activity encountered in clinical practice is epilepsy.
Generalized and continuous electrical discharges of the cortex (crisis) are associated with coma, even in the absence of epileptic motor activity (convulsions). Coma following seizures, called the postictal state, may be due to the depletion of energy metabolites or may be secondary to the local production of toxic molecules during attacks. The return from postictal insensitivity occurs at the restoration of neuronal metabolic balance.
The postictal state produces a pattern of continuous, generalized slowdown in the activity of basic EEG, similar to that of metabolic encephalopathy.
Let's finish this post with the patient's approach... Diagnosis and immediate intervention in a coma depend on the knowledge of the main causes of clinical practice, the interpretation of certain clinical signs, the reflexes of the brain stem and the efficient use of diagnostic tests.
It is well known that acute cardiovascular and respiratory problems should be considered prior to neurological diagnosis. Full medical examination, excluding vital signs, butt examination and nucal stiffness examination, may be postponed until the neurological evaluation has determined the severity and nature of the comet.
In many cases, the cause of the comet is immediately obvious (e.g. trauma, cardiac arrest, ingestion of known drugs), otherwise the anamnestic information related to the onset of the comet is often poor. The most useful anamnestic landmarks are: 1. circumstances and temporal profile of the onset of neurological symptoms, 2. precise details of the preceding neurological symptoms (confusion, weakness, headache, seizures, dizziness, diplopia or vomiting), 3. use of illegal drugs, medicines or alcohol and 4. liver, kidney, lung, heart or other medical conditions. Phones to family or immediate observers are important factors in the initial assessment. Those who work on the ambulance often provide the best information in an enigmatic case.
In the case of physical examination and general observations, the first steps are to measure temperature, pulse, respiratory frequency and blood pressure. Fever suggests a systemic infection, bacterial meningitis, encephalitis or brain damage that disrupted temperature control centers.
A high temperature, 42-44 degrees Celsius, associated with dry skin, should arouse suspicion of sunstroke or intoxication with anticholinergic drugs. Hypothermia is observed in low temperature exposure, alcohol poisoning, barbiturates or phenothiasdes, hypoglycaemia, peripheral circulation disorders or hypothyroidism. Hypothermia itself produces coma only if the temperature is below 31 degrees Celsius.
Outlier respiratory patterns that may reflect disorders of brain stem function are relevant. A change in heart rate combined with hyperventilation and hypertension may signal an increase in intracranial pressure. Significant hypertension is a very important sign of hypertensive encephalopathy, cerebral hemorrhage or hydrocephalus and occurs acutely, but at a lower level, after head trauma.
Hypotension is characteristic in alcoholic coma or barbiturate intoxication, internal bleeding, myocardial infarction, septicaemia and Addisonian crisis. Examination of the bottom of the eye is useful in detecting subarachnoid haemorrhage (subhialoid haemorrhage), hypertensive encephalopathy (exudated, haemorrhages, changes in the cross-vessel) and increased intracranial pressure (papillary oedema). Generalized skin spots suggest thrombocytopenic thrombotic purpura or a hemorrhagic diathesis associated with intracerebral hemorrhage.
We'll continue tomorrow with the patient's approach, starting with the general neurological evaluation.
Let's get on with it! The reduction of wakefulness is dependent in a semi-quantitative manner on the total mass of the injured cortex or reticulated activator system (RAS) and is not represented in focus in any region of the hemispheres, except that the large, acute and unilateral damage to a hemisphere, especially the left hemisphere, may cause transient dizziness even in the absence of damage to the contralateral hemisphere or the SRA.
Hemispheric lesions, in most cases, cause coma in an indirect way when a large tumor mass in one or both hemispheres compresses the secondary upper brain stem and diencephalic SRA. This is characteristic for brain haemorrhages and rapidly expansive tumors. The degree of limitation of wakefulness is also related to the suddenness of the installation of brain dysfunction or SRA compression.
This compressive side effect led to the concept of transtentorial hernia, with progressive dysfunction of the brain stem, to explain the neurological signs of coma caused by lesions caused by supratentorial mass. Herniation refers to moving brain tissue towards mass, passing a less mobile structure like hard, and placing it in a space that it doesn't normally occupy.
The usual hernias observed postmortem are transfacial (displacement of the cingulate gir under the scythe of the brain in the anterior median line), transtentorial (median temporal lobe displaced in the tentorial opening) and foraminal (forced cerebellar tonsils in the occipital hole).
Central transtentorial hernia denoting a symmetrical downward motion of the upper diencephalus (talamic region) by the tentorial opening in the median line and is suggested by myosis and dizziness. It is considered that these changes in the brain can cause a progression of the compression of the rosral brain stem to the caudal, first of the mesencephalus, then of the bridge and finally of the bulb, leading to the sequential appearance of neurological signs corresponding to the affected level and progressive decrease in alertness.
However, many patients with supratentorial mass do not follow these stereotypical patterns, for example, an orderly progression of signs from mesencephalus to bulb is rarely observed in the case of major lesions, in which all brain functions are lost almost simultaneously.
Moreover, dizziness and stupor typically occur with moderate lateral changes in the diencephalus, when there is only minimal vertical displacement of structures near the tentoral opening and before the downward hernia is evident at TC or MRI scan.
Now you can move on to a few presentation of a few "things" about the physiopathology of come and confusion. Coma of metabolic origin is produced by interrupting the supply of energy substrate (hypoxia, ischemia, hypoglycaemia) or by altering the neurophysiological responses of neural membranes (drug or alcohol poisoning, toxic endogenous metabolites, anesthesia or epilepsy).
The same metabolic abnormalities can cause generalized neuronal dysfunction in the cortex, which diminishes all mental aspects and causes an acute confusional state. In this way, acute confusion and coma can be seen as a continuous metabolic encephalopathy.
The brain is dependent on continuous cerebral blood flow (FSC), oxygen and glucose. The brain's glucose reserves provide energy for about 2 minutes after blood flow is interrupted and consciousness is lost within 8-10 seconds.
When hypoxia is installed simultaneously with ischemia, glucose in reserves is consumed much faster. When the average FSC drops below one-third of the normal average, the EEG is diffusely slowed (typical for metabolic encephalopathy) and when it drops below about one-fifth the electrical activity of the brain ceases. If all other conditions, such as temperature and arterial oxygenation, remain normal, with an FSC lowered below about one-seventh of normal, irreversible brain damage is achieved.
The rapidity of enlargement and the duration of ischemia are also major determinants of irreversible impairment. Coma and confusion due to hyponatremia, hyperosmolarity, hypercapnia, hypercalcemia and renal or hepatic encephalopathy are associated with a variety of metabolic disorders of neurons and astrocytes.
The reversible toxic effects of these disorders on the brain are not well understood, but can, in various cases, disrupt energy reserves, change ion flows through the neural membrane and cause abnormalities in neurotransmission.
For example, increased concentrations of brain ammonia associated with hepatic coma interfere with brain energy metabolism, and the ATP-acase pump of Na+ and K+ increases the number and size of astrocytes, causes increased concentrations of potentially toxic ammonia metabolism products and produces neurotransmitter abnormalities, including possible "false" neurotransmitters, which can act competitively at the receiving site.
Ammonia and other metabolites may also bind to gamma-aminobutyric-acid receptors, leading to CNS depression through endogenous mechanisms. Moreover, these changes are not exclusively reciprocal.
The mechanism of encephalopathy in renal failure is also very little understood. Unlike ammonia, urea itself does not produce toxicity to the central nervous system (CNS). A multifactorial cause is possible, including increased permeability of the blood-brain barrier to toxic substances such as organic acids and an increase in cerebral calcium or phosphate content of cerebrospinal fluid (CRL). Osmolarity abnormalities are involved in coma and seizures caused by several systemic medical disorders, including diabetic ketoacidosis, noncetosic hyperosmolarity and hyponatremia.
The volume of water in the brain best correlates with the level of consciousness in the hyperosmolar-hyponatremic state, but there are probably other factors that play a role. Low sodium levels are associated with acute or sub acute confusion and severely reduced levels are associated with coma and seizures, depending on the rapidity with which hyponatremia develops.
Hipepappnia produces a decreased level of consciousness, proportional to the pressure of carbon dioxide in the blood and the suddenness of the onset. A correlation has been established between CRL acidosis and the severity of symptoms.
The physiology of other metabolic encephalopathy such as hypercalcemia, hypothyroidism, vitamin B12 deficiency and hypothermia are poorly understood, but should also reflect disorders in CNS biochemistry and membrane function. It turns out that the large group of CNS depressive drugs, anesthetics and some endogenous toxins produce coma through suppression of both the SRA and the cerebral cortex.
For this reason, combinations of signs of damage to the brain stem occur in the overdose of drugs and other metabolic comets, which can lead to the specific diagnosis of structural lesion of the brain stem. Although all metabolic disorders alter neuronal electrophysiology, the only main disorder of electrical brain activity encountered in clinical practice is epilepsy.
Generalized and continuous electrical discharges of the cortex (crisis) are associated with coma, even in the absence of epileptic motor activity (convulsions). Coma following seizures, called the postictal state, may be due to the depletion of energy metabolites or may be secondary to the local production of toxic molecules during attacks. The return from postictal insensitivity occurs at the restoration of neuronal metabolic balance.
The postictal state produces a pattern of continuous, generalized slowdown in the activity of basic EEG, similar to that of metabolic encephalopathy.
Let's finish this post with the patient's approach... Diagnosis and immediate intervention in a coma depend on the knowledge of the main causes of clinical practice, the interpretation of certain clinical signs, the reflexes of the brain stem and the efficient use of diagnostic tests.
It is well known that acute cardiovascular and respiratory problems should be considered prior to neurological diagnosis. Full medical examination, excluding vital signs, butt examination and nucal stiffness examination, may be postponed until the neurological evaluation has determined the severity and nature of the comet.
In many cases, the cause of the comet is immediately obvious (e.g. trauma, cardiac arrest, ingestion of known drugs), otherwise the anamnestic information related to the onset of the comet is often poor. The most useful anamnestic landmarks are: 1. circumstances and temporal profile of the onset of neurological symptoms, 2. precise details of the preceding neurological symptoms (confusion, weakness, headache, seizures, dizziness, diplopia or vomiting), 3. use of illegal drugs, medicines or alcohol and 4. liver, kidney, lung, heart or other medical conditions. Phones to family or immediate observers are important factors in the initial assessment. Those who work on the ambulance often provide the best information in an enigmatic case.
In the case of physical examination and general observations, the first steps are to measure temperature, pulse, respiratory frequency and blood pressure. Fever suggests a systemic infection, bacterial meningitis, encephalitis or brain damage that disrupted temperature control centers.
A high temperature, 42-44 degrees Celsius, associated with dry skin, should arouse suspicion of sunstroke or intoxication with anticholinergic drugs. Hypothermia is observed in low temperature exposure, alcohol poisoning, barbiturates or phenothiasdes, hypoglycaemia, peripheral circulation disorders or hypothyroidism. Hypothermia itself produces coma only if the temperature is below 31 degrees Celsius.
Outlier respiratory patterns that may reflect disorders of brain stem function are relevant. A change in heart rate combined with hyperventilation and hypertension may signal an increase in intracranial pressure. Significant hypertension is a very important sign of hypertensive encephalopathy, cerebral hemorrhage or hydrocephalus and occurs acutely, but at a lower level, after head trauma.
Hypotension is characteristic in alcoholic coma or barbiturate intoxication, internal bleeding, myocardial infarction, septicaemia and Addisonian crisis. Examination of the bottom of the eye is useful in detecting subarachnoid haemorrhage (subhialoid haemorrhage), hypertensive encephalopathy (exudated, haemorrhages, changes in the cross-vessel) and increased intracranial pressure (papillary oedema). Generalized skin spots suggest thrombocytopenic thrombotic purpura or a hemorrhagic diathesis associated with intracerebral hemorrhage.
We'll continue tomorrow with the patient's approach, starting with the general neurological evaluation.
Sunday
full of understanding, love and gratitude but also fresh air,
fun and what else you can manage to attract into your life!
Dorin, Merticaru