STUDY - Technical - New Dacian's Medicine
Acute
Confusion and Coma (4)
Translation Draft
Respiratory patterns have received a lot of attention in the diagnosis of come, but they have an inconsistent localization value. Shallow, slow, well-tuned breathing suggests metabolic or drug depression. Deep rapid breathing (Kussmaul) usually involves metabolic acidosis, but can also occur in pontomesencephalic lesions. Cheyne-Stokes breathing in its cyclic form, ending with a short apneic period, signifies mild biemispheric injury or metabolic depression and normally accompanies mild coma.
The agonic gâfing reflects bilateral damage to the lower brain stem and is well known as terminal respiratory patterns of a very severe brain disorder. In patients with "dead brain", movements similar to shallow, non-repetitive back-arcing, irregular, can be produced by hypoxia and are likely generated by the surviving cervical marrow and lower bulb. Other cyclic respiratory variations are not commonly diagnosed for specific local lesions.
Let me now present the patient's approach with acute confusion. Acute confusion is characterized by the difficulty of maintaining a coherent flow of mental thought and performance. Attention can be assessed by the clarity and speed of the response during the anamnesis, but it should also be examined by having the patient repeat strings of numbers (most adults easily retain 7 digits in ascending order and 4 in descending order) or perform series of calculations that require the retention of the result one calculation in the working memory before moving on to the next step (the test with 3 to 30 decreases in series is a common paradigm).
Guidance and memory are tested by asking the patient in an open manner the date, including the month, day, year and day of the week, the indication of the space and some general knowledge data and universally known information (the name of the president, a recent national catastrophe, the capital of the state).
In the subsequent examination it may be necessary to highlight a defect (why the patient is there, what is his address, identification code, telephone number, etc.). Problems of greater complexity may occur when patients provide little practical information once the confusion has been established.
Proof of ingestion of medicines should be examined on general physical examination. Other silent neurological signs are the level of alertness, which fluctuates characteristically in acute cases being signs of outbreak of cerebellum lesion, such as hemiparesis, hemianopsia and, in particular, aphasia, spontaneous movements of myoclonia or seizures.
The most relevant sign of metabolic encephalopathy is the asterixis, an arrhythmic tremor wave, which is typically obtained by requiring the patient to hold the perfectly straight hand with the fist joint in full extension. After a few seconds there is a fall with great tremors in the position of the hand, and then a quick return to the original position. The same aspect can be appreciated in any sustained tonic position, even of the tongue and, in extreme forms, movements can disturb the voluntary mobility of the limb.
Bilateral asterixis always signifies metabolic encephalopathy, for example, from liver failure or after drug ingestion especially anticonvulsants. Myoclonic spasm and tremor in a awake patient are typical for uremic encephalopathy or ingestion of antipsychotropic drugs.
The language of a confused patient can be disorganized and divastated, even with extension to paraphasic words. These characteristics, together with the alteration of the capacity for understanding due to inattention, may be misinterpreted as aphasia.
The distinction between dementia and confusion is a big problem. Memory loss from dementia necessarily causes a confusional state that varies in severity from hour to hour and from day to day. The decrease in mental performance derives in particular from incomplete concentration, inadequate access to names and ideas and the inability to retain new information, thus affecting effective orientation and understanding (attention is maintained in the early stages of the process).
Depending on the nature of dementia disease, specific language deficits, praxis, visual performance (spatial or a slow frontal lobe state) may be added. Finally, dementia causes chronic confusion, with the collapse of all types of mental performance and the distinction of confusion depends, simply, on the chronic nature of the condition.
In general, laboratory examinations in acute confusion and coma consist of chemical and toxicological analysis of blood and urine, TC or MRI, EEC and CRL examination. Chemical blood determinations are performed routinely to investigate metabolic, toxic or drug-induced encephalopathy.
In clinical practice there are major changes in blood levels of electrolytes, calcium, urea, glucose, changes in plasma osmolarity and liver dysfunction (especially related to ammonia). Toxicological analysis is of great value in any case of coma in which the diagnosis is not immediately clear. However, the presence of exogenous drugs or toxins, especially alcohol, cannot guarantee that other factors, in particular head trauma, do not also contribute to the clinical condition.
Increased availability of TC and MRI focused attention on the causes of comet that are radiologically identifiable (e.g. haemorrhages, tumors or hydrocephalus). This approach, although sometimes expeditious, is imprudent, since many cases of confusion and coma have a metabolic or toxic origin. The idea that a normal TC excludes anatomical lesions as the cause of the comet is also flawed.
Early bilateral espheric infarction, small lesions of the brain stem, encephalitis, meningitis, mechanical sectioning of axons as a result of a closed head trauma, absent cerebral infusion associated with brain death, sagittal sinus thrombosis and subdural hematomas that are isolated to the adjacent brain are some of the lesions that can be escaped on the TC examination.
Even MRI can fail in highlighting these early processes in their developments. However, in coma of unknown etiology, TC or MRI should be performed. In cases where the etiology is clinically evident, they ensure verification and define the extent of the lesion.
In the case of lesions caused by the existence of a tumor mass, the horizontal displacement of 3 to 5 mm of the pineal body from the median line corresponds to dizziness, by 5 to 8 mm corresponds to the stupor and greater than 8 mm of the comet. As the supratentorial mass increases, the opposite perimesencephalic tank is first compressed by the lateral movement of the brain stem, the ipsilateral tank is enlarged and finally both are compressed by the effects of the lateral tumor mass.
The lateral ventricle opposite the mass widens as the third ventricle is compressed. These radiological characteristics of tissue movements near the tentoral opening are helpful in linking the clinical state with the progress of a tumor lesion visible through scanning. For technical reasons, MRI is difficult to perform in comatous patients and also does not highlight bleeding as well as TC. EEG is useful in metabolic or drug-induced confusional states, but rarely has diagnostic value in coma, except for comets due to clinically unrecognized seizures, herpes encephalitis and Creutzfeldt-Jakob disease.
The size of the background slowdown of the EEG is a useful landmark of the severity of any diffuse encephalopathy. The predominant high voltage slowdown (delta waves) in the frontal regions is typical for metabolic coma, such as that of liver failure. and diffuse rapid activity (beta) involves the effects of sedative drugs.
The EG pattern of "alpha come" is defined by the invariant activity of 8 to 12 Hz diffuse, superficially similar to the normal alpha rhythm of the waking state, but which does not respond to environmental stimuli. Coma alpha results either from a superior pontine injury or from a diffuse cortical lesion and is associated with an unfavorable prognosis.
Coma due to persistent epileptic discharges that are not clinically manifest may be revealed by THE EGE records. Normal alpha activity on the EEG may also suggest the clinician's blockage syndrome, or a case of hysteria.
Computerized analysis of the EEG and records of the potential caused (auditory and somatosensory) are useful as additional methods of diagnosis and monitoring of the comet. The lumbar puncture is now used more judiciously in cases of coma or confusion, because TC excludes intracerebral haemorrhages and most subarachnoid haemorrhages. The use of lumbar puncture in a coma is limited to the diagnosis of encephalitis/ meningitis and suspected subarachnoid haemorrhage cases in which TC is normal. Lumbar puncture should not be delayed if meningitis is an almost definite clinical possibility.
That's enough for today! Tomorrow I will complete the confusion and coma by addressing the elements of differential diagnosis, treatment and prognosis.
Respiratory patterns have received a lot of attention in the diagnosis of come, but they have an inconsistent localization value. Shallow, slow, well-tuned breathing suggests metabolic or drug depression. Deep rapid breathing (Kussmaul) usually involves metabolic acidosis, but can also occur in pontomesencephalic lesions. Cheyne-Stokes breathing in its cyclic form, ending with a short apneic period, signifies mild biemispheric injury or metabolic depression and normally accompanies mild coma.
The agonic gâfing reflects bilateral damage to the lower brain stem and is well known as terminal respiratory patterns of a very severe brain disorder. In patients with "dead brain", movements similar to shallow, non-repetitive back-arcing, irregular, can be produced by hypoxia and are likely generated by the surviving cervical marrow and lower bulb. Other cyclic respiratory variations are not commonly diagnosed for specific local lesions.
Let me now present the patient's approach with acute confusion. Acute confusion is characterized by the difficulty of maintaining a coherent flow of mental thought and performance. Attention can be assessed by the clarity and speed of the response during the anamnesis, but it should also be examined by having the patient repeat strings of numbers (most adults easily retain 7 digits in ascending order and 4 in descending order) or perform series of calculations that require the retention of the result one calculation in the working memory before moving on to the next step (the test with 3 to 30 decreases in series is a common paradigm).
Guidance and memory are tested by asking the patient in an open manner the date, including the month, day, year and day of the week, the indication of the space and some general knowledge data and universally known information (the name of the president, a recent national catastrophe, the capital of the state).
In the subsequent examination it may be necessary to highlight a defect (why the patient is there, what is his address, identification code, telephone number, etc.). Problems of greater complexity may occur when patients provide little practical information once the confusion has been established.
Proof of ingestion of medicines should be examined on general physical examination. Other silent neurological signs are the level of alertness, which fluctuates characteristically in acute cases being signs of outbreak of cerebellum lesion, such as hemiparesis, hemianopsia and, in particular, aphasia, spontaneous movements of myoclonia or seizures.
The most relevant sign of metabolic encephalopathy is the asterixis, an arrhythmic tremor wave, which is typically obtained by requiring the patient to hold the perfectly straight hand with the fist joint in full extension. After a few seconds there is a fall with great tremors in the position of the hand, and then a quick return to the original position. The same aspect can be appreciated in any sustained tonic position, even of the tongue and, in extreme forms, movements can disturb the voluntary mobility of the limb.
Bilateral asterixis always signifies metabolic encephalopathy, for example, from liver failure or after drug ingestion especially anticonvulsants. Myoclonic spasm and tremor in a awake patient are typical for uremic encephalopathy or ingestion of antipsychotropic drugs.
The language of a confused patient can be disorganized and divastated, even with extension to paraphasic words. These characteristics, together with the alteration of the capacity for understanding due to inattention, may be misinterpreted as aphasia.
The distinction between dementia and confusion is a big problem. Memory loss from dementia necessarily causes a confusional state that varies in severity from hour to hour and from day to day. The decrease in mental performance derives in particular from incomplete concentration, inadequate access to names and ideas and the inability to retain new information, thus affecting effective orientation and understanding (attention is maintained in the early stages of the process).
Depending on the nature of dementia disease, specific language deficits, praxis, visual performance (spatial or a slow frontal lobe state) may be added. Finally, dementia causes chronic confusion, with the collapse of all types of mental performance and the distinction of confusion depends, simply, on the chronic nature of the condition.
In general, laboratory examinations in acute confusion and coma consist of chemical and toxicological analysis of blood and urine, TC or MRI, EEC and CRL examination. Chemical blood determinations are performed routinely to investigate metabolic, toxic or drug-induced encephalopathy.
In clinical practice there are major changes in blood levels of electrolytes, calcium, urea, glucose, changes in plasma osmolarity and liver dysfunction (especially related to ammonia). Toxicological analysis is of great value in any case of coma in which the diagnosis is not immediately clear. However, the presence of exogenous drugs or toxins, especially alcohol, cannot guarantee that other factors, in particular head trauma, do not also contribute to the clinical condition.
Increased availability of TC and MRI focused attention on the causes of comet that are radiologically identifiable (e.g. haemorrhages, tumors or hydrocephalus). This approach, although sometimes expeditious, is imprudent, since many cases of confusion and coma have a metabolic or toxic origin. The idea that a normal TC excludes anatomical lesions as the cause of the comet is also flawed.
Early bilateral espheric infarction, small lesions of the brain stem, encephalitis, meningitis, mechanical sectioning of axons as a result of a closed head trauma, absent cerebral infusion associated with brain death, sagittal sinus thrombosis and subdural hematomas that are isolated to the adjacent brain are some of the lesions that can be escaped on the TC examination.
Even MRI can fail in highlighting these early processes in their developments. However, in coma of unknown etiology, TC or MRI should be performed. In cases where the etiology is clinically evident, they ensure verification and define the extent of the lesion.
In the case of lesions caused by the existence of a tumor mass, the horizontal displacement of 3 to 5 mm of the pineal body from the median line corresponds to dizziness, by 5 to 8 mm corresponds to the stupor and greater than 8 mm of the comet. As the supratentorial mass increases, the opposite perimesencephalic tank is first compressed by the lateral movement of the brain stem, the ipsilateral tank is enlarged and finally both are compressed by the effects of the lateral tumor mass.
The lateral ventricle opposite the mass widens as the third ventricle is compressed. These radiological characteristics of tissue movements near the tentoral opening are helpful in linking the clinical state with the progress of a tumor lesion visible through scanning. For technical reasons, MRI is difficult to perform in comatous patients and also does not highlight bleeding as well as TC. EEG is useful in metabolic or drug-induced confusional states, but rarely has diagnostic value in coma, except for comets due to clinically unrecognized seizures, herpes encephalitis and Creutzfeldt-Jakob disease.
The size of the background slowdown of the EEG is a useful landmark of the severity of any diffuse encephalopathy. The predominant high voltage slowdown (delta waves) in the frontal regions is typical for metabolic coma, such as that of liver failure. and diffuse rapid activity (beta) involves the effects of sedative drugs.
The EG pattern of "alpha come" is defined by the invariant activity of 8 to 12 Hz diffuse, superficially similar to the normal alpha rhythm of the waking state, but which does not respond to environmental stimuli. Coma alpha results either from a superior pontine injury or from a diffuse cortical lesion and is associated with an unfavorable prognosis.
Coma due to persistent epileptic discharges that are not clinically manifest may be revealed by THE EGE records. Normal alpha activity on the EEG may also suggest the clinician's blockage syndrome, or a case of hysteria.
Computerized analysis of the EEG and records of the potential caused (auditory and somatosensory) are useful as additional methods of diagnosis and monitoring of the comet. The lumbar puncture is now used more judiciously in cases of coma or confusion, because TC excludes intracerebral haemorrhages and most subarachnoid haemorrhages. The use of lumbar puncture in a coma is limited to the diagnosis of encephalitis/ meningitis and suspected subarachnoid haemorrhage cases in which TC is normal. Lumbar puncture should not be delayed if meningitis is an almost definite clinical possibility.
That's enough for today! Tomorrow I will complete the confusion and coma by addressing the elements of differential diagnosis, treatment and prognosis.
Don't forget to have a
good day!
Dorin, Merticaru