STUDY - Technical - New Dacian's Medicine
Acute
Confusion and Coma (5)
Translation Draft
So let's move on to the differential diagnosis of confusion and coma! In most cases, confusion and coma are part of an obvious medical problem, such as known drug ingestion, hypoxia, stroke, trauma or renal or hepatic failure. Attention is primarily focused on primary (substantive) disease.
A complete list of all the diseases that cause confusion and coma would not be of much help, because it would not help in diagnosis, but some general rules are useful. Diseases leading to a sudden or acute coma are due to ingestion of medicines or catastrophic brain damage (haemorrhage, trauma, hypoxia or rare occlusion of the basilar artery).
Coma that occurs subacutely is generally related to previous medical or neurological problems, including secondary cerebral edema surrounding a pre-existing lesion. Diagnosis of comethe therefore requires a certain familiarity with frequent major intracerebral accidents.
These can be summarized in: 1. talamic haemorrhage and basal ganglia (acute but not with an instant onset, vomiting, headache, hemiplegia and characteristic ocular signs), 2. subarachnoid haemorrhage (instant onset, severe headache, neck stiffness, vomiting, lesions to the 3rd and 6th nerve, transient loss of consciousness or sudden coma with strong extensor position), 3. Pontine haemorrhage (sudden onset, pupils like needle tip, loss of reflex eye movements and corneal response, "eye pendulum", hyperventilation and sweating), 4. cerebellar haemorrhage (occipital headache, vomiting, fixed-looking paresis and inability to stand) and 5. basilar arterial thrombosis (neurological prodrom or alarm disorders, diplopia, dysartria, vomiting and eye movements and abnormal corneal response and asymmetrical paresis of the limbs).
The most common stroke, especially heart attack in the territory of the middle cerebral artery, does not lead to acute coma. Acute hydrocephalus syndrome causing coma may accompany major intracranial accidents, especially subarachnoid hemorrhage. Acute symmetrical dilation of both lateral ventricles leads to headache and sometimes vomiting followed by dizziness, which can rapidly progress to coma, with extensor posture of the limbs, bilateral Babinski signs, small pupils active and abnormal oculocephal vertical movements.
If the diagnosis and examination are not typical for any neurological diagnosis and metabolic or medicinal causes are excluded, then the information obtained by TC or MRI can be used (TC being useful in differential diagnosis and due to accuracy and the fact that it is easily accessible).
With regard to craniocerebral post-trauma coma, cerebral concussion is a common form of transient coma, resulting from the twisting of the hemispheres around the mesencephal-diencephalus junction with a short discontinuation of SRA function. The main causes are subdural or epidural hemorrhage, deep cerebral hemorrhage, bilateral frontotemporal contusions and extensive damage to the white substance.
In the case of coma with ischemic-anoxic damage to the brain, there are generalized and complex changes in the CNS following cardiac arrest or after deep hypotension or anoxia. Some of these are physiological and mediated by alterations in electrical function and neurotransmission, and others may result from the endogenous release of neurotoxins that ultimately lead to neuronal death.
It differentiates several clinically recognized models, which usually occur in pure form but which may coexist: 1. a deep coma with the preservation of the function of the brain stem that evolves into vegetative state or dementia, reflecting damage to the function of neurons along the cortex (the brain stem can be suppressed in the early hours, thus rivalling brain death and the limbs can be flasce, either have a strong posture of extension or myoclonic contractions) , 2. sympathic or paraparetic proximal weakness syndromes or cortical blindness, which are due to bilateral infarctions of the regions between the territories of cortical vessels by decreasing blood flow, 3. an amnesiac condition Korsakoff indicating vulnerability of neurons in the hippocampal cortex and, rarely, 4. a cerebellar syndrome.
Brain death results from complete cessation of cerebral blood flow and overall brain infarction during artificial maintenance of breathing, with the heart continuing to function. It is the only case of irrevocable loss of current brain function recognized by law as the equivalent of death.
Several sets of equivalent criteria for the diagnosis of brain death have been advanced, requiring the most locally approved and recognized as standard in medical practice. The ideal criteria are those that are simple, determined at the patient's bedside and that do not give the possibility of diagnostic error.
There are three essential elements: 1. extensive cortical destruction demonstrated by deep coma, 2. global damage to the brain stem demonstrated by the absence of pupil reaction to light and by the absence of oculovestibular and corneal reflexes and 3. bulbar destruction indicated by complete apnea. Pulse rate is also invariable and nonresponsive to atropine.
Most patients have diabetes insipidus, but in some it develops under the clinical signs of brain death. Pupils need not be fully dilated, but they do not need to be contracted. The absence of deep tendinous reflexes is not necessary, because the spinal cord can remain functional.
The possibility of deep depression of drug-induced CNS or caused by hypothermia should always be excluded. It is desirable a period of observation, usually 6 to 24 hours, during which this state is maintained. It is often advisable to postpone clinical testing for up to 24 hours if the heart attack was the cause of brain death or if the determining disease is not known.
Large lesions in the posterior fossa that compress the brain stem, CNS depressant drugs and deep hypothermia can simulate brain death, but proper use of protocols can prevent errors. Isoelectric EEG is often used as a test to confirm total cortical damage, but it is not necessarily necessary.
Brain scans with radioisotopes, cerebral angiography or transcranial Doppler measurements can also be used to demonstrate the absence of cerebral blood flow but, with the exception of the Doppler test, are hard to reach. There is no explicit reason to diagnose brain death unless the question of organ transplantation is or when the necessary intensive therapy is difficult to provide.
Although it is normally accepted that the ventilation device can be disconnected from a patient with brain death, many problems arise due to the impossibility of fully explaining the phenomenon and its causes and requires the preparation of the family by the doctor.
Let us now proceed to the presentation of several elements related to the treatment of acute confusional states and comet. The immediate purpose in acute coma is to prevent further cns damage. Hypotension, hypoglycaemia, hypercalcemia, hypoxia, hypercapnia and hyperthermia should be quickly and carefully corrected. To keep pharynx open in wet patients who breathe normally, it is advisable to install an oropharyngeal device.
Tracheal intubation is indicated in case of apnea, obstruction of the upper airways, hypoventilation or emesis, or if the patient needs to be vacuumed. Mechanical ventilation is required if the patient has hypoventilation or if there is an intracranial mass and induced hypocapnia is required.
Intravenous access is established and naloxone and dextrose are administered if narcotic overdose or hypoglycaemia have been excluded. Thiamine is generally administered with glucose to prevent an exacerbation of Wernicke encephalopathy in malnourished patients. The veins of people who abuse intravenous drugs are difficult to cantoanate, in such cases naloxone being injected sublingually through a small needle.
In case of suspected basilar thrombosis with cerebral stem ischemia, intravenous heparin or a thrombolytic agent after TC is administered, given that cerebellar and pontine haemorrhage resemble scare syndrome for basilar arterial occlusion. Physiostigmine, when used by an experienced physician under close monitoring, can wake patients with cholinergic drug overdose, but many doctors believe that this is only justified to treat associated cardiac arrhythmias due to these overdoses.
The use of benzodiazepine antagonists is promising in the treatment of overdoses and has a transient benefit in hepatic encephalopathy. Intravenous water administration should be carefully monitored in any acute severe CNS disease due to the danger of exacerbation of intracranial edema.
Neck injuries should not be overlooked, especially when intubation or oculocephal manoeuvre is intended. Headache accompanied by fever and meningism indicates the urgent need for an examination of CRL for the diagnosis of meningitis and the lumbar puncture should not be postponed to wait for TC.
Dilation of a pupil usually indicates secondary compression in the mesencephalus by a tumor in a hemisphere and requires immediate reduction of intracranial pressure (PIC). Surgical evacuation of the tumor may be necessary. Medical conduct to reduce intracranial pressure consists of intravenous administration of normosalin fluid (most definitely intravenous fluid in all patients because it is slightly hyperosmolar).
Therapeutic hyperventilation can be used but the effects are short-lived. Hyperosmolar therapy with mannitol or equivalent is essential in reducing intracranial pressure. In critical cases, it can be used simultaneously with hyperventilation. Ventricular puncture is necessary to decompress hydrocephalus if medical measures fail to awaken.
Clinical studies have not shown that the increased dose of barbiturates and other neuronal sparing agents immediately after cardiac arrest would be beneficial and corticosteroids were not of value, except in cases of brain tumors.
I will complete this series of posts with the prognosis of the come and vegetative state. The importance of predicting the evolution of the comet is determined by the allocation of medical resources and the limitation of support in hopeless cases. To this day, no collection of clinical signs, except those from brain death, can certainly predict the evolution of a come, but certain groups have prognostic value.
Children and young adults may initially show threatening clinical signs, such as abnormal reflexes of the brain stem, and yet recover. It is therefore necessary that all prognostic schemes be considered as approximate indicators, and medical decision should take into account other factors such as age, underlying disease, general condition of the body.
In an attempt to collect forecast information from a large number of patients with head injuries, a scale called Glasgow was developed which has empirically predictive values in case of craniocerebral trauma. The main points indicate 95% mortality rate in patients whose pupil reaction or reflex eye movements are absent 6 hours after the onset of the comet and 91% if the pupils are active at 24 hours (although 5% recover very well).
The prognosis of non-traumatic comet is difficult due to the heterogeneity of the determining diseases. In general, metabolic coma has a more favorable prognosis than hypoxic or traumatic coma. unfavorable signs in the first hours after admission are the absence of two of the three signs: pupil reaction, corneal reflex, oculo-vestibular response.
The day after the onset of the comet, the signs presented above, together with the absence of eye opening and muscle tone, predict death or severe incapacity, and the third day the same signs reinforce the unfavorable prognosis. In many patients, precise combinations of predictive signs do not appear, and the coma scales lose their value.
The use of evoked potentials helps to establish the prognosis in patients with cranio-cerebral trauma or post-heart coma. The bilateral absence of evoked somato-sensitive cortical evokes is associated with death or vegetative state in most cases.
Doctors are less lysitable in withdrawing the support of patients who are not dead but who have serious neurological damage as the criteria for prognosis become more trustworthy and resources are increasingly scarce.
The prognosis regarding the total recovery of mental faculties after the installation of a vegetative state is almost null. Most cases of spectacular recovery, when thoroughly investigated, lead to the usual rules of prognosis, but it should be noted that rare cases of recovery after months or years of vegetative state with sequelae of the type of dementia or paralysis have been documented.
I'm ready!!! Have a good day!
So let's move on to the differential diagnosis of confusion and coma! In most cases, confusion and coma are part of an obvious medical problem, such as known drug ingestion, hypoxia, stroke, trauma or renal or hepatic failure. Attention is primarily focused on primary (substantive) disease.
A complete list of all the diseases that cause confusion and coma would not be of much help, because it would not help in diagnosis, but some general rules are useful. Diseases leading to a sudden or acute coma are due to ingestion of medicines or catastrophic brain damage (haemorrhage, trauma, hypoxia or rare occlusion of the basilar artery).
Coma that occurs subacutely is generally related to previous medical or neurological problems, including secondary cerebral edema surrounding a pre-existing lesion. Diagnosis of comethe therefore requires a certain familiarity with frequent major intracerebral accidents.
These can be summarized in: 1. talamic haemorrhage and basal ganglia (acute but not with an instant onset, vomiting, headache, hemiplegia and characteristic ocular signs), 2. subarachnoid haemorrhage (instant onset, severe headache, neck stiffness, vomiting, lesions to the 3rd and 6th nerve, transient loss of consciousness or sudden coma with strong extensor position), 3. Pontine haemorrhage (sudden onset, pupils like needle tip, loss of reflex eye movements and corneal response, "eye pendulum", hyperventilation and sweating), 4. cerebellar haemorrhage (occipital headache, vomiting, fixed-looking paresis and inability to stand) and 5. basilar arterial thrombosis (neurological prodrom or alarm disorders, diplopia, dysartria, vomiting and eye movements and abnormal corneal response and asymmetrical paresis of the limbs).
The most common stroke, especially heart attack in the territory of the middle cerebral artery, does not lead to acute coma. Acute hydrocephalus syndrome causing coma may accompany major intracranial accidents, especially subarachnoid hemorrhage. Acute symmetrical dilation of both lateral ventricles leads to headache and sometimes vomiting followed by dizziness, which can rapidly progress to coma, with extensor posture of the limbs, bilateral Babinski signs, small pupils active and abnormal oculocephal vertical movements.
If the diagnosis and examination are not typical for any neurological diagnosis and metabolic or medicinal causes are excluded, then the information obtained by TC or MRI can be used (TC being useful in differential diagnosis and due to accuracy and the fact that it is easily accessible).
With regard to craniocerebral post-trauma coma, cerebral concussion is a common form of transient coma, resulting from the twisting of the hemispheres around the mesencephal-diencephalus junction with a short discontinuation of SRA function. The main causes are subdural or epidural hemorrhage, deep cerebral hemorrhage, bilateral frontotemporal contusions and extensive damage to the white substance.
In the case of coma with ischemic-anoxic damage to the brain, there are generalized and complex changes in the CNS following cardiac arrest or after deep hypotension or anoxia. Some of these are physiological and mediated by alterations in electrical function and neurotransmission, and others may result from the endogenous release of neurotoxins that ultimately lead to neuronal death.
It differentiates several clinically recognized models, which usually occur in pure form but which may coexist: 1. a deep coma with the preservation of the function of the brain stem that evolves into vegetative state or dementia, reflecting damage to the function of neurons along the cortex (the brain stem can be suppressed in the early hours, thus rivalling brain death and the limbs can be flasce, either have a strong posture of extension or myoclonic contractions) , 2. sympathic or paraparetic proximal weakness syndromes or cortical blindness, which are due to bilateral infarctions of the regions between the territories of cortical vessels by decreasing blood flow, 3. an amnesiac condition Korsakoff indicating vulnerability of neurons in the hippocampal cortex and, rarely, 4. a cerebellar syndrome.
Brain death results from complete cessation of cerebral blood flow and overall brain infarction during artificial maintenance of breathing, with the heart continuing to function. It is the only case of irrevocable loss of current brain function recognized by law as the equivalent of death.
Several sets of equivalent criteria for the diagnosis of brain death have been advanced, requiring the most locally approved and recognized as standard in medical practice. The ideal criteria are those that are simple, determined at the patient's bedside and that do not give the possibility of diagnostic error.
There are three essential elements: 1. extensive cortical destruction demonstrated by deep coma, 2. global damage to the brain stem demonstrated by the absence of pupil reaction to light and by the absence of oculovestibular and corneal reflexes and 3. bulbar destruction indicated by complete apnea. Pulse rate is also invariable and nonresponsive to atropine.
Most patients have diabetes insipidus, but in some it develops under the clinical signs of brain death. Pupils need not be fully dilated, but they do not need to be contracted. The absence of deep tendinous reflexes is not necessary, because the spinal cord can remain functional.
The possibility of deep depression of drug-induced CNS or caused by hypothermia should always be excluded. It is desirable a period of observation, usually 6 to 24 hours, during which this state is maintained. It is often advisable to postpone clinical testing for up to 24 hours if the heart attack was the cause of brain death or if the determining disease is not known.
Large lesions in the posterior fossa that compress the brain stem, CNS depressant drugs and deep hypothermia can simulate brain death, but proper use of protocols can prevent errors. Isoelectric EEG is often used as a test to confirm total cortical damage, but it is not necessarily necessary.
Brain scans with radioisotopes, cerebral angiography or transcranial Doppler measurements can also be used to demonstrate the absence of cerebral blood flow but, with the exception of the Doppler test, are hard to reach. There is no explicit reason to diagnose brain death unless the question of organ transplantation is or when the necessary intensive therapy is difficult to provide.
Although it is normally accepted that the ventilation device can be disconnected from a patient with brain death, many problems arise due to the impossibility of fully explaining the phenomenon and its causes and requires the preparation of the family by the doctor.
Let us now proceed to the presentation of several elements related to the treatment of acute confusional states and comet. The immediate purpose in acute coma is to prevent further cns damage. Hypotension, hypoglycaemia, hypercalcemia, hypoxia, hypercapnia and hyperthermia should be quickly and carefully corrected. To keep pharynx open in wet patients who breathe normally, it is advisable to install an oropharyngeal device.
Tracheal intubation is indicated in case of apnea, obstruction of the upper airways, hypoventilation or emesis, or if the patient needs to be vacuumed. Mechanical ventilation is required if the patient has hypoventilation or if there is an intracranial mass and induced hypocapnia is required.
Intravenous access is established and naloxone and dextrose are administered if narcotic overdose or hypoglycaemia have been excluded. Thiamine is generally administered with glucose to prevent an exacerbation of Wernicke encephalopathy in malnourished patients. The veins of people who abuse intravenous drugs are difficult to cantoanate, in such cases naloxone being injected sublingually through a small needle.
In case of suspected basilar thrombosis with cerebral stem ischemia, intravenous heparin or a thrombolytic agent after TC is administered, given that cerebellar and pontine haemorrhage resemble scare syndrome for basilar arterial occlusion. Physiostigmine, when used by an experienced physician under close monitoring, can wake patients with cholinergic drug overdose, but many doctors believe that this is only justified to treat associated cardiac arrhythmias due to these overdoses.
The use of benzodiazepine antagonists is promising in the treatment of overdoses and has a transient benefit in hepatic encephalopathy. Intravenous water administration should be carefully monitored in any acute severe CNS disease due to the danger of exacerbation of intracranial edema.
Neck injuries should not be overlooked, especially when intubation or oculocephal manoeuvre is intended. Headache accompanied by fever and meningism indicates the urgent need for an examination of CRL for the diagnosis of meningitis and the lumbar puncture should not be postponed to wait for TC.
Dilation of a pupil usually indicates secondary compression in the mesencephalus by a tumor in a hemisphere and requires immediate reduction of intracranial pressure (PIC). Surgical evacuation of the tumor may be necessary. Medical conduct to reduce intracranial pressure consists of intravenous administration of normosalin fluid (most definitely intravenous fluid in all patients because it is slightly hyperosmolar).
Therapeutic hyperventilation can be used but the effects are short-lived. Hyperosmolar therapy with mannitol or equivalent is essential in reducing intracranial pressure. In critical cases, it can be used simultaneously with hyperventilation. Ventricular puncture is necessary to decompress hydrocephalus if medical measures fail to awaken.
Clinical studies have not shown that the increased dose of barbiturates and other neuronal sparing agents immediately after cardiac arrest would be beneficial and corticosteroids were not of value, except in cases of brain tumors.
I will complete this series of posts with the prognosis of the come and vegetative state. The importance of predicting the evolution of the comet is determined by the allocation of medical resources and the limitation of support in hopeless cases. To this day, no collection of clinical signs, except those from brain death, can certainly predict the evolution of a come, but certain groups have prognostic value.
Children and young adults may initially show threatening clinical signs, such as abnormal reflexes of the brain stem, and yet recover. It is therefore necessary that all prognostic schemes be considered as approximate indicators, and medical decision should take into account other factors such as age, underlying disease, general condition of the body.
In an attempt to collect forecast information from a large number of patients with head injuries, a scale called Glasgow was developed which has empirically predictive values in case of craniocerebral trauma. The main points indicate 95% mortality rate in patients whose pupil reaction or reflex eye movements are absent 6 hours after the onset of the comet and 91% if the pupils are active at 24 hours (although 5% recover very well).
The prognosis of non-traumatic comet is difficult due to the heterogeneity of the determining diseases. In general, metabolic coma has a more favorable prognosis than hypoxic or traumatic coma. unfavorable signs in the first hours after admission are the absence of two of the three signs: pupil reaction, corneal reflex, oculo-vestibular response.
The day after the onset of the comet, the signs presented above, together with the absence of eye opening and muscle tone, predict death or severe incapacity, and the third day the same signs reinforce the unfavorable prognosis. In many patients, precise combinations of predictive signs do not appear, and the coma scales lose their value.
The use of evoked potentials helps to establish the prognosis in patients with cranio-cerebral trauma or post-heart coma. The bilateral absence of evoked somato-sensitive cortical evokes is associated with death or vegetative state in most cases.
Doctors are less lysitable in withdrawing the support of patients who are not dead but who have serious neurological damage as the criteria for prognosis become more trustworthy and resources are increasingly scarce.
The prognosis regarding the total recovery of mental faculties after the installation of a vegetative state is almost null. Most cases of spectacular recovery, when thoroughly investigated, lead to the usual rules of prognosis, but it should be noted that rare cases of recovery after months or years of vegetative state with sequelae of the type of dementia or paralysis have been documented.
I'm ready!!! Have a good day!
Dorin, Merticaru