D.3. Relación entre la eliminación de segmentos abdominales y la rotación genital del macho
D.3.2. La rotación de la placa genital desde un punto de vista no autónomo de disco
Etiology/Risk Factors
• Head Trauma
• Depressed skull fracture
• Subdural hematoma, intracerebral hemorrhage
• Infectious
• Meningitis, encephalitis, abscess
• Vascular
• Stroke or vascular malformations
• Hypertensive encephalopathy
• Eclampsia
• Environmental
• Hyperthermia
• Toxic
• Drug overdose or withdrawal
• Neoplasm
• Metabolic
• Hypoglycemia
• Hypo- or hypernatremia
• Hypo- or hypercalcemia
• Uremia; hepatic encephalopathy
• Hyperosmolar states
• Congenital
• Idiopathic epilepsy
• Hematologic
• Porphyria
• Neurologic
• Febrile seizures
• HIV encephalopathy
• Global cerebral ischemia
Scope of the Problem
• Nearly 1% of all emergency department visits are due to new-onset generalized sei-zures in adults. Seizure may be the sole presenting symptom of a life-threatening ill-ness requiring immediate treatment.
• Seizures are defined as disordered discharges of cerebral neurons. The outward expres-sion of a seizure may take many forms:
• Generalized seizures involve a loss of consciousness.
• Tonic-clonic seizures are characterized by a phase of tonic muscle contractions causing extension of the limbs (and falling) and cessation of ventilatory effort, followed by a clonic phase of rhythmic muscle contraction and relaxation resulting in symmet-ric jerking of the limbs with return of spontaneous respirations. Urinary inconti-nence may occur. A postictal phase of unconsciousness or confusion is not uncom-mon. It usually clears within 30 min, but may last for hours.
• Absence seizures are characterized by a brief (5-10 second) loss of consciousness, during which postural tone is maintained. Blinking or head turning may be the only motor manifestation of the seizure. There is no postictal period of confusion.
• Partial Seizures
• Simple partial seizures begin within a specific region of the cortex, which deter-mines the symptoms (i.e., sensory, motor, or autonomic). The symptoms may
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sponteously resolve, recur, spread to contiguous cortical regions (jacksonian march), or become secondarily generalized. In the absence of generalization, there is no loss of consciousness.
• Complex partial seizures cause impaired consciousness. Patients experience the same symptoms during each successive ictal event. The episode classically begins with a blank stare, and (occasionally) loss of muscle tone, resulting in a fall. Epigastric sensations are most common, but affective, cognitive, or sensory symptoms also occur. Automatisms are common and can be simple (e.g., chewing, blinking, laugh-ing) or complex (e.g., vocalizations or repetitive movments). Secondary generaliza-tion may occur so rapidly that the preceding partial component is not recognized, and only the altered mental status is observed. A postictal period is common but usually short (i.e., minutes).
Diagnosis
History• If the seizure activity has terminated prior to the patient’s arrival in the emergency department, a description of the event from a reliable witness is invaluable. Any his-tory of trauma (recent or remote) should be elicited. A description of events immedi-ately preceding the seizure activity should also be sought, including any complaints of pain or focal neurologic deficits. Attempt to determine whether the patient was in-jured during the episode (e.g., fall).
• Obtain the patient’s medical history, if possible, including a prior history of seizures or other medical conditions, medications, or recent symptoms (e.g., infections). Ask about the use of drugs or alcohol, or exposure to other toxins.
Physical Examination
• Include a rectal temperature with the vital signs.
• Look for evidence of trauma, either as a cause or a result of the seizure. A detailed neuro-logic examination should be performed. If the patient has an altered level of conscious-ness, is he in a postictal state? Or is there another cause? Are there any focal neurologic deficits? Look for signs of increased intracranial pressure (ICP) (e.g., papilledema). Is there evidence of a CNS or systemic infection? Are there other signs of systemic illness?
Is there evidence of a toxic exposure? Serial neurologic exams are critical.
Differential Diagnosis
Toxic and metabolic Hypoglycemia; renal or hepatic dysfunction encephalopathies with Recreational drug use; alcoholic blackouts fluctuating consciousness Delerium tremens
Syncope Neurocardiogenic; vasovagal; orthostatic; cardiac Cerebrovascular TIA (incl. vertebrobasilar insufficiency) Movement disorders Dystonias
Tonic spasms with tetanus, strychnine, and camphor Tic disorders; tremor
Benign nocturnal myoclonus Asterixis with hepatic and renal failure Rabies
Transient global amnesia
Migraine (including acephalgic migraine)
Paroxysmal endocrine Pheochromocytoma; carcinoid syndrome disturbances
Sensory disturbances Visual hallucinations with visual field loss Paroxysmal vertigo
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Sleep disorders Apnea
Night terrors; sleep walking Narcolepsy; hypersomnia
Psychogenic Hyperventilation; breath-holding spells in children Panic attacks; episodic dyscontrol; dissociative states Conversion disorder; hysteria; malingering; psychosis Obsessive-compulsive disorder
Pseudoseizure
Evaluation
As with the work-up of any presenting sign(s) or symptom(s), the use of diagnos-tic tests should be guided by the history and physical examination of each patient who presents with seizure activity. When a differential diagnosis is formulated for a particular patient, the following studies may be helpful in ruling in or excluding specific etiologies:
• Laboratory
• Glucose should be checked on all first-time seizure patients. Although commonly ordered, routine electrolytes, calcium and magnesium have low diagnostic yield in otherwise healthy patients with a first seizure. Consider these studies when clini-cally indicated.
• A pregnancy test is indicated in all females of reproductive age.
• Antiepileptic drug (AED) levels
• A more extensive work-up is appropriate in patients with a history of alcohol abuse, to include CBC, PT, electrolytes, BUN, and creatinine. A blood alcohol level and toxicology screen should also be considered.
• Magnesium levels should also be checked in patients with diabetic ketoacidosis.
• Coagulation studies are recommended in patients on anticoagulants, with a known coagulopathy, or with a history of platelet disorders.
• Lumbar puncture is indicated in the following situations:
• Persistent alteration in mental status or status epilepticus (after patient is stabi-lized).
• Signs of CNS infection (nuchal rigidity, petechiae)
• Severe headache (i.e., when unruptured aneurysm or SAH is suspected)
• In a patient with a history of cancer and negative CT scans (leptomeningeal metastases?)
• History of immunosuppression, without an identifiable cause for the seizure (i.e., lab or radiographic abnormality)
• Children with recent antibiotic use
• Adults with fever, without an infectious source (neutropenic patients excluded)
• Imaging
• Emergent noncontrast CT scan of the head is indicated in all first-time seizure patients without an identifiable, nonstructural cause (e.g., hypoglycemia, febrile seizure). The following factors increase the likelihood of an abnormal CT:
• A focally abnormal exam or signs of increased ICP
• Multiple or focal seizures
• Higher likelihood of structural abnormalities (i.e., increased age, history of head trauma, HIV/other immunocompromised states, cancer, alcohol abuse, antico-agulation, vascular disease, demographic risk of cysticercosis)
• Previous CNS disorders
• Subtherapeutic antiepileptic drug levels are the most common cause of recurrent seizures. Indications for CT scan in patients with a previously diagnosed seizure disorder include:
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• Change in seizure pattern without a known cause
• Persistently altered mental status or prolonged postictal confusion
• New focal neurologic deficits
• Contrast-enhanced head CT should be performed in immunocompromised patients and those with a history of malignancy (after a negative noncontrast CT).
• MRI is recommended, on an elective basis, if the screening CT is negative.
• EEG
• EEG is generally not readily available in the ED and usually is not required in the ED work-up of seizures. However, in the following cases, emergent EEG is indicated:
• The seizure appears to have terminated, but the patient remains altered.
• Status epilepticus is suspected (convulsive or nonconvulsive).
• EKG
• Seizure may be the presenting symptom of hypoxia in a patient with a dysrhythmia resulting from myocardial ischemia. EKG should be considered in patients with known or suspected coronary artery disease.
• Patients with long QT syndrome frequently present after a syncopal or ictal event.
Congenital long QT syndrome is seen in children or young adults who may have a family history of syncope or early cardiac death, or a personal history of congenital deafness. Long QT syndrome may be acquired and is a side effect of tricyclic antide-pressants, phenothiazines, and amiodarone. Associated EKG abnormalities include prolonged or abnormal T waves and bradycardia.
Treatment
• As with any patient in the ED, attention to the patient’s airway, breathing, and circu-lation is paramount. The patient should be positioned in such a way as to protect the airway in case of vomiting, and suction should be readily available. Supplemental oxygen should be administered by nasal cannula or face mask, and the patient placed on continuous pulse oximetry.
• If trauma is a concern, the cervical spine should be immobilized.
• As soon as possible, intravenous or intraosseous access should be obtained so that fluids and medications can be given. The patient should be placed on a cardiac monitor.
• Underlying, correctable etiologies should be rapidly identified and treated.
• Benzodiazepines are the agents of choice to acutely terminate seizure activity, although the necessity of this practice as routine is debatable. Most seizures are brief (<2 min) and there is no evidence that a single, brief seizure has deleterious central nervous system effects. Several agents are available (see Table 4G.1).
• Diazepam is highly lipophilic and thus crosses the blood-brain barrier rapidly. It is usually administered via the intravenous route but is equally effective when given rectally. Other routes include oral and endotracheal. The median time to terminate seizure activity after injection is 2 min. However, its antiepileptic activity lasts only 20 to 30 min. Depending upon the clinical setting, a longer acting AED may be necessary after administration of diazepam.
• Lorazepam is less lipid soluble than diazepam but has a similar time to seizure control (3 min). Its antiepileptic activity lasts 12-24 h, negating the need to admin-ister an additional AED if seizure activity is terminated. Acceptable routes of ad-ministration include intravenous, rectal, sublingual, and oral.
• Midazolam is used less frequently but is another option. Unlike diazepam and lorazepam, this agent is well absorbed when given via the intramuscular route be-cause of its water-solubility. After administration, it becomes lipid soluble and, like diazepam, has rapid penetration of the blood-brain barrier as well as a short dura-tion of antiepileptic activity. Acceptable routes of administradura-tion include intrana-sal, intramuscular, intravenous, rectal, and buccal.
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• Initiation of a long-term AED for a first seizure should be considered in certain settings.
Close neurologic follow-up is indicated for these patients. All AEDs have adverse side effects and “label” the patient. If there is any question as to the necessity of initiating chronic therapy, neurologic consultation is advised. Multiple AEDs are available—a com-prehensive discussion is beyond the scope of this writing. Consider initiation of an AED in the following cases:
• An underlying cause that can’t be promptly treated (e.g., tumor)
• A patient at risk for recurrent seizures (e.g., cysticercosis, penetrating head injury)
• Presence of an identifiable, remote cause (debatable)
• Patients with a history of recent (<2 yr) seizure that went untreated