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Antipsychotics are a structurally diverse group of heterocyclic compounds; more than 50 different drugs are available for clinical use worldwide with numerous others are in various stages of development discount neurontin 600mg line symptoms 3 days dpo. Classes include benzamide buy 800 mg neurontin free shipping medicine 2632, benzepine order 800 mg neurontin free shipping treatment, butyrophenone (phenylbutylpiperidine), dibenzo-oxepino pyrrole, diphenylbutylpiperidine, indole, phenothiazine, quinolinone, rauwolfia alkaloid, and thioxanthene derivatives (Table 105. The phenothiazine and thioxanthene classes are further subdivided into three groups (aliphatic, piperazine, and piperidine) based on central ring side- chain substitution. Although traditionally classified by structure, antipsychotics are more ideally classified by pharmacologic profile. Newer agents that have minimal extrapyramidal side effects at clinically effective antipsychotic doses are effective for treating the negative symptoms (e. The characterization of antipsychotics as typical or atypical is ultimately determined by receptor binding. One or more of several different receptor-binding characteristics are associated with drug atypia, and each agent is atypical for different reasons . Understanding how specific receptor-binding characteristics produce clinical effects has facilitated the development of antipsychotics that separate antipsychotic activity from other activities; thus, minimizing adverse effects and maximizing patients’ compliance. Antipsychotic toxicity may occur as an idiosyncratic reaction during therapeutic use or following accidental or intentional overdose. Most deaths are the consequence of suicidal overdose by psychotic or depressed adults and frequently involve mixed ingestions or ingestion of the agents chlorpromazine, loxapine, mesoridazine, quetiapine, or thioridazine [10,11]. From one study, the most toxic antipsychotics result in death from poisoning for every 100 patient-years of use . For both classes of drugs, the risk of sudden cardiac death increases significantly with an increasing dose. Initially, dopaminergic neurons increase the synthesis and release of dopamine in response to autoreceptor antagonism. With repeated dosing, however, depolarization inactivation of the neuron occurs, and decreased synthesis and release of dopamine occur despite ongoing postsynaptic receptor blockade. All antipsychotics produce their therapeutic antipsychotic effect from mesolimbic D -receptor antagonism. D -receptor affinity (potency) in2 2 this region strongly correlates with the daily therapeutic dose (see Table 105. Simultaneous antagonism of other D receptors produces2 additional clinical effects, the majority of which are undesirable. Mesocortical receptor blockade appears to create cognitive impairment and further worsens the negative symptoms of schizophrenia. D -receptor blockade in the anterior hypothalamus (preoptic area) may2 alter core temperature set point and block thermosensitive neuronal inputs and thermoregulatory responses. D -receptor blockade in the pituitary (tuberoinfundibular2 pathway) results in sustained elevated prolactin secretion, which may cause galactorrhea, gynecomastia, menstrual changes, and sexual dysfunction (impotence in men) . The antiemetic activity of antipsychotics results from similar inhibition of dopaminergic receptors in the chemoreceptor trigger zone (area postrema) of the medulla oblongata. Antagonism of dopamine receptors presents on peripheral sympathetic nerve terminals and vascular smooth muscle cells may produce autonomic dysfunction (i. The ratio of other neuroreceptor-binding affinities to D -receptor–binding2 affinity (relative binding affinity) predicts the likelihood of producing those receptor-mediated effects at clinically effective antipsychotic (D -2 blocking) doses and with overdose . Significant relative α -adrenergic blockade,2 as occurs with asenapine, clozapine, paliperidone, and risperidone, may result in sympathomimetic effects (e. Olanzapine, clozapine, and aliphatic and piperidine phenothiazines are associated with clinically significant anticholinergic effects. The ability of clozapine to produce sialorrhea is likely mediated by its partial agonism at M and1 M receptors [4 1]. The advent of atypical agents, which provide an improved motor side- effect profile, marks significant progress in the neuroleptic development. Atypical agents may be subdivided into four functional groups: (a) the D - and D -receptor antagonists (i. Conversely, typical antipsychotics are characterized by high D -receptor potency 2 (low-milligram dosing) and a narrow receptor profile in the brain . Unlike typical agents, atypical agents also appear to have a minimal propensity to elevate serum prolactin concentrations. Sodium-channel blockade is voltage and frequency dependent; blockade is augmented at less negative membrane potentials and faster heart rates . Potassium-channel blockade is concentration-, voltage-, and reverse-frequency dependent; blockade is increased at higher tissue concentrations, less negative membrane potentials, and slower heart rates . Potassium-channel blockade may result in early after depolarizations and subsequent torsade de pointes (TdP)–type ventricular tachycardia. Haloperidol, mesoridazine, thioridazine, and pimozide share an added property of calcium-channel blockade . Electrophysiologic effects variably include a depressed rate of phase 0 depolarization, depressed amplitude and duration of phase 2, and prolongation of phase 3 repolarization. Cardiac effects are dose and concentration dependent but can occur with therapeutic as well as toxic doses. Ventricular tachyarrhythmias and asphyxia (caused by seizures, aspiration, or respiratory depression) have been postulated as etiologies of sudden death for patients taking therapeutic doses of antipsychotics, particularly phenothiazines [9,25]. Antipsychotics produce dose-related electroencephalographic changes, and some agents have been shown to lower the seizure threshold [26,27]. The mechanism by which antipsychotics produce seizures is not well understood but likely involves dose-related blockade of norepinephrine reuptake, antagonism of γ- aminobutyric acid type A receptors, and altered neuronal transmembrane ionic currents. Tablet, capsule, and liquid oral preparations, suppository, and injectable immediate-release and sustained-release (depot) solutions are available. Oral preparations include both rapidly disintegrating (sublingual absorption) and sustained-release formulations. Paliperidone, the active metabolite of risperidone, is commercially available in an extended-release oral preparation (Invega). Following a single dose, plasma concentrations gradually rise and do not peak until approximately 24 hours after dosing . When administered orally, they are well absorbed, but bioavailability is unpredictable (range 10% to 70%) owing to large interindividual variability and presystemic (hepatic and intestinal) metabolism [29,30]. After parenteral administration, drug bioavailability is 4 to 10 times greater than with oral dosing because of the absence of first-pass metabolism [29,30]. After oral overdose, absorption should occur more rapidly (first-order kinetics), but peak plasma concentrations are delayed, because more time is required for complete absorption. However, because they are also highly lipophilic, volumes of distribution are large (10 to 40 L per kg), and serum drug levels after therapeutic doses are quite low (one to several hundred ng per mL). These pharmacokinetic characteristics make extracorporeal removal by hemodialysis or hemoperfusion impractical.
If the cords can be seen best buy neurontin medicine 801, the defective tube is removed under direct visualization and reintubation is performed using the new tube order neurontin line medications knee. If the cords cannot be seen on direct laryngoscopy purchase neurontin in india medications safe in pregnancy, the tube can be changed over an airway exchange catheter (e. Factors implicated in the etiology of complications include tube size, characteristics of the tube and cuff, trauma during intubation, duration and route of intubation, metabolic or nutritional status of the patient, tube motion, and laryngeal motor activity. Possible complications include aspiration; damage to teeth and dental work; corneal abrasions; perforation or laceration of the pharynx, larynx, or trachea; dislocation of an arytenoid cartilage; retropharyngeal perforation; epistaxis; hypoxemia; myocardial ischemia; laryngospasm with noncardiogenic pulmonary edema; and death [2,3]. Many of these complications can be avoided by paying careful attention to technique and ensuring that personnel with the greatest skill and experience perform the intubation. The presence of acute respiratory failure and shock appears to be an independent risk factor for the occurrence of complications in the latter setting [42,43]. Bradyarrhythmias can also be observed and are probably caused by stimulation of the laryngeal branches of the vagus nerve. In the patient with myocardial ischemia, short-acting agents to control blood pressure (nitroprusside and nicardipine) and heart rate (esmolol) during intubation may be needed. The sudden appearance of blood in tracheal secretions suggests anterior erosion into overlying vascular structures, and the appearance of gastric contents suggests posterior erosion into the esophagus. Both situations require urgent bronchoscopy, and it is imperative that the mucosa underlying the cuff be examined. Placing a bite block in the patient’s mouth can minimize occlusion of the tube caused by the patient biting down on it. Judicious use of sedatives and analgesics and appropriately securing and marking the tube can minimize these problems. Ulcerations of the lips, mouth, or pharynx can occur and are more common if the initial intubation was traumatic. Irritation of the larynx appears to be caused by local mucosal damage and occurs in as many as 45% of individuals after extubation. Unilateral or bilateral vocal cord paralysis is an uncommon but serious complication following extubation. In children, however, even a small amount of edema can compromise the already small subglottic opening. Laryngeal granulomas and synechiae of the vocal cords are extremely rare, but these complications can seriously compromise airway patency. Technique of Extubation the patient should be alert, lying with the head of the bed elevated to at least a 45-degree angle. The cuff is deflated, and positive pressure is applied to expel any foreign material that has collected above the cuff as the tube is withdrawn. In situations in which postextubation difficulties are anticipated, equipment for emergency reintubation should be assembled at the bedside. In addition, administration of preextubation steroids will reduce the risk of developing stridor . Some clinicians have advocated the “leak test” as a means to predict the risk of stridor after extubation. The utility of this procedure is limited in routine practice, but for patients with certain risk factors (e. Probably, the safest way to extubate the patient if there are concerns about airway edema or the potential need to reintubate a patient with a difficult airway is to use an airway exchange catheter. Supplemental oxygen can be provided via the catheter to the patient, and the catheter can be used as a stent for reintubation if necessary. One of the most serious complications of extubation is laryngospasm, and it is more likely to occur if the patient is not fully conscious. Succinylcholine can cause severe hyperkalemia in a variety of clinical settings; therefore, only clinicians who are experienced with its use should administer it. Ventilation with a mask and bag unit is needed until the patient has recovered from the succinylcholine. Utility of Ultrasonography for Airway Management Ultrasonography has several useful applications related to airway management. Identification of Gastric Fluid Ultrasonography examination of the stomach is a useful means of identifying gastric contents . With the phased array probe configured for abdominal scanning, the examination is performed with longitudinal (coronal) scanning plane over the lower left lateral thorax in the midaxillary line. An alternative method is to examine the left upper quadrant from the anterior approach, although gas artifact frequently blocks adequate imaging. If the patient is so unstable that this is not possible, the team, alerted to the risk of massive aspiration, may take specific steps to reduce this risk, such as utilization of a paralytic agent, preparing extra suction devices, and assigning the intubation to the team member with highest skill level. The high-frequency vascular transducer is used to obtain a transverse-axis image of the trachea immediately above the suprasternal notch (Video 8. The anterior wall of the trachea appears as a curvilinear echogenic line often in association with a posterior comet tale artifact. Jaber S, Jung B, Corne P, et al: An intervention to decrease complications related to endotracheal intubation in the intensive care unit: a prospective, multiple-center study. Nouruzi-Sedeh P, Schumann M, Groeben H: Laryngoscopy via Macintosh blade versus GlideScope: success rate and time for endotracheal intubation in untrained medical personnel. Barjaktarevic I, Berlin D: Bronchoscopic intubation during continuous nasal positive pressure ventilation in the treatment of hypoxemic respiratory failure. Miguel-Montanes R, Hajage D, Messika J, et al: Use of high-flow nasal cannula oxygen therapy to prevent desaturation during tracheal intubation of intensive care patients with mild-to-moderate hypoxemia. Akihisa Y, Hoshijima H, Maruyama K, et al: Effects of sniffing position for tracheal intubation: a meta-analysis of randomized controlled trials. Subirana M, Sola I, Benito S: Closed tracheal suction systems versus open tracheal suction systems for mechanically ventilated adult patients. In the early 1900s, this procedure was used to treat difficult cases of respiratory paralysis from poliomyelitis. Largely because of improvements in tubes and advances in clinical care, endotracheal intubation has become the treatment of choice for short-term airway management. Although urgent tracheostomy or emergent cricothyrotomy is occasionally required in critically ill and injured patients who cannot be intubated for various reasons (e. With improvements in critical care medicine over the past 30 years, more patients are surviving their initial episodes of acute respiratory failure, trauma, and extensive surgeries, and require prolonged periods of mechanical ventilation. In this chapter, we review the indications, contraindications, complications, and techniques associated with tracheostomy. There are several advantages and disadvantages of both translaryngeal intubation and tracheostomy in patients requiring prolonged ventilator support, and these are summarized in Table 9. Most authors feel that when the procedure is performed by a skilled specialist, the potential benefits of tracheostomy over translaryngeal intubation for most patients justify the application despite its potential risks.
While awake discount 800mg neurontin free shipping medicine 3 times a day, neither obtunded nor stuporous patients demonstrate a normal content of consciousness order neurontin 800mg without prescription medications voltaren, but both may display purposeful movements 300 mg neurontin overnight delivery treatment zinc toxicity, attempting to ward off painful stimuli or to remove catheters, endotracheal tubes, or intravenous lines. Patients in coma are unresponsive to suprathreshold sensory stimulation, including noxious stimulation that is strong enough to arouse a deeply sleeping patient but not strong enough to cause physical injury. Although the patient usually lies motionless, movements such as stereotyped, inappropriate postures (decerebration and decortication) and spinal cord reflexes (triple flexion and Babinski responses) may occur. Irrespective of the etiology, the duration of coma is typically no longer than 2 to 4 weeks, after which one of the three conditions supervenes: arousal to full or partial recovery, a vegetative state, or death. Most of the literature on prognosis of comatose patients comes from nontraumatic coma, largely anoxic–ischemic brain injury. A landmark paper by Levy, Plum, and associates from 1981 established the neurologic examination—particularly absence of brainstem reflexes including pupillary, corneal, and oculocephalic reflexes—as important predictors of poor outcome in nontraumatic coma . Multiple studies followed which confirmed the importance of motor responses in addition to brainstem examination, and some diagnostic tests were established as useful in predicting outcomes; these are well summarized in the American Academy of Neurology Practice Parameter on post-cardiopulmonary resuscitation by Wijdicks et al. Given the life-or- death responsibility of the physician providing a prognosis, only clinical indicators or diagnostic tests that are highly specific with a near-zero false-positive rate are utilized. A poor outcome is predicted by the absence of pupillary and corneal reflexes, absent or extensor motor responses, absent responses to caloric testing of the oculovestibular reflex at day 3 post-arrest, and the presence of myoclonic status epilepticus on day 1 post-arrest. Prognostication must include consideration of the etiology of the disease process, the clinical examination findings, and radiologic evidence of damage to the upper pons, midbrain, diencephalon, and other vital structures for arousal. Psychogenic unresponsiveness may be suggested by active resistance or rapid closure of the eyelids, pupillary constriction to visual threat, fast phase of nystagmus (i. Caloric testing with ice water irrigation of the ear will elicit a normal nystagmoid response with the fast phase directed away from the irrigated ear, and possibly some nausea and vomiting. Psychiatric conditions that may be associated with psychogenic coma are conversion reactions secondary to hysterical personality, severe depression, or acute situational reaction, catatonic schizophrenia, dissociative or fugue states, severe psychotic depression, and malingering. Because the most common cause of this state is destruction of the base of the pons, the patient is completely paralyzed except for muscles subserved by midbrain structures (i. The most frequent cause is cerebrovascular such as cerebral infarction from a basilar thromboembolism, or pontine hemorrhage from uncontrolled hypertension; less frequent etiologies of the syndrome are acute polyneuropathy (Guillain–Barré syndrome), acute poliomyelitis, or toxins that block transmission at the neuromuscular junction. It is important to note that locked-in patients are capable of hearing, seeing, and feeling external stimuli and pain. Adequate analgesia and anxiolysis should be provided despite the absence of external signs of pain and anxiety. A 5- to 10-year survival has been reported in as high as 80% of patients in some series and a surprising 58% of patients surveyed reported satisfaction with life despite their disability in a small case series . Brain Death the term brain death refers to a determination of physical death by brain-based, rather than cardiopulmonary-based, criteria . Brain death is the irreversible destruction of the brain, with the resulting total absence of all cortical and brainstem function, although spinal cord reflexes may remain [10,11]. It is not to be confused with severe but incomplete brain damage with a poor prognosis or with a vegetative state, conditions in which some function of vital brain centers still remains. In brain death, support of other organs is futile for the patient, whereas when there is some residual brain or brainstem function, or a vegetative state, decisions regarding ongoing life support clearly depend on the wishes of the patient or his or her proxy. Brain death may be simulated by drug intoxications and cannot be evaluated when toxic drugs are present; depending on preserved renal and hepatic function, most such toxic effects do not persist longer than 36 hours. Hypothermia also precludes a diagnosis of brain death, and the patient must be brought to normal temperature prior to declaring death. Unresponsiveness that can mimic brain death may occur with extensive brainstem destruction, for example, after basilar artery thrombosis. Exclusion of complicating medical conditions that may confound clinical assessment (no severe electrolyte, acid–base, or endocrine disturbance) 3. Coma, and absence of motor responses including decerebrate posturing, although spinal reflexes may be seen 2. The criteria take into account etiology, performance of two separate clinical examinations 6 hours apart, and include the method of apnea testing with preoxygenation and oxygen . As criteria for brain death vary from state to state, and procedures to determine brain death differ among institutions, it is important to be familiar with the guidelines in your institution . The occurrence of brain death provides the opportunity for organ donation, and most institutions have a protocol that includes informing organ bank organizations to facilitate this. Patient Who Appears Confused Confusion is a general term used for patients who do not think with customary speed, clarity, or coherence. The causes of this condition include among others an acute confusional state, toxic encephalopathies, dementia, inapparent seizures, and receptive aphasia. Acute Confusional State When the cerebral hemispheres are negatively affected by toxic, metabolic, anoxic, structural, or infectious processes, the patient may appear acutely confused [13,14]. Poor arousal and an abnormal content of consciousness may contribute to the clinical presentation, and the etiologies are legion (Table 145. Their processing of information is slow and effortful, state of consciousness fluctuates from drowsiness to hyperexcitability, attention span is poor, and recall and recent memory are impaired. If sensorial clouding becomes more advanced, sensory input is increasingly misinterpreted, daytime drowsiness alternates with nocturnal agitation, disorientation for place and time becomes apparent, and repeated prompting is required for a response to even the simplest commands. Delirious patients typically manifest acutely fluctuating confusion, with psychomotor overactivity, agitation, autonomic instability, and often visual hallucinations. Clinical observations frequently suggest that the disturbance of cognition or perception is directly related to a potentially reversible general medical condition rather than to an evolving dementia. Signs of autonomic overactivity include pupillary dilatation, diaphoresis, tachycardia, and hypertension. Patients with delirium may not sleep, sometimes for periods of several days; the success of treatment can be judged by the development of normal sleep. Delirium tremens, the most serious consequence of ethanol withdrawal, is perhaps the best- known example of this state. In beclouded dementia, confusion is superimposed on an underlying subacute or chronic cognitive disorder. The preexisting cerebral dysfunction may be mental retardation, dementia, or the deficits from a vascular, neoplastic, or demyelinative process. In some cases, the underlying disorder is not diagnosed until the confusion appears during an intercurrent illness (e. Dementia Patients with dementia have subacute or chronic intellectual dysfunction unaccompanied by a reduction in arousal . The patient exhibits a decline in multiple cognitive functions, including memory, language, spatial orientation, personality, abstract thinking, and insight. The ability to carry out testing requires relative preservation of attention and language comprehension. Careful observation may alert the clinician to seizure phenomena, such as episodic staring, eye deviation or nystagmoid jerks, facial or hand clonic activity, and automatisms. Nonconvulsive status epilepticus should be considered, and is the cause of otherwise unexplained coma in as many as 8% of patients . A benzodiazepine, such as diazepam or lorazepam, or an anticonvulsant drug may eliminate the discharge and improve the patient’s state of consciousness.
In a retrospective and a nonrandomized study discount neurontin 800 mg symptoms enlarged prostate, there were conflicting data on mortality in patients with respiratory failure of more than 1 week with regard to receiving a tracheostomy or continuing with an endotracheal tube [1 cheap neurontin treatment yeast infection,2] order neurontin 400 mg with visa medications zolpidem. However, a prospective cohort study has demonstrated that percutaneous tracheostomy can be safely preformed in patients with refractory coagulopathy from liver disease . In patients with severe brain injury, percutaneous tracheostomy can be safely performed without significantly further increasing intracranial pressure . In patients undergoing conversion from translaryngeal intubation to a tracheostomy for prolonged ventilatory support, the procedure should be viewed as an elective or semielective procedure. Therefore, the patient should be optimally physiologically stabilized before the procedure, and all attempts should be made to correct coagulopathies, including uremia. The patient should tolerate submaximal ventilator settings because during the exchange positive pressure is lost temporarily. Emergent tracheostomies for upper airway obstruction may need to be performed when the patient is unstable or has a coagulopathy. However, with the release of some consistent and recent studies, more sound recommendations can be made. In 2003, Heffner recommended consideration of tracheostomy if a patient remains ventilator dependent after a week of translaryngeal intubation. If the patient has barriers to weaning and appears unlikely to be extubated within 7 days, a tracheostomy should be performed. Conversely, if the patient has minimal barriers to weaning and is likely to be extubated within 7 days, tracheostomy should be avoided. Potential reasons for the decrease in duration of mechanical ventilation include easier weaning due to less dead space; lower airflow resistance; and less frequent episodes of obstruction due to mucus plugging in patients with tracheostomies. However, there were limitations to the meta-analysis, including the inclusion of insufficiently randomized studies. Since this meta-analysis, multiple randomized controlled studies have been published which have consistently contradicted these results . Patients were identified by Intensive Care Day 4, as likely to require mechanical ventilation for at least an additional 7 days, and subsequently randomized to either group. Median critical care unit length of stay and need for antibiotics were similar in the groups, whereas the median days of intravenous sedation was lower in the early group: 5 versus 8 days, p < 0. Delayed tracheostomy likely leads to avoidance of trachoestomy in many patients, and correspondingly avoidance of potential complications associated with the procedure. Early tracheostomy may be beneficial in some specific instances; however, the majority of the data is based on retrospective studies. Patients with blunt, multiple-organ trauma have a shorter duration of mechanical ventilation, fewer episodes of nosocomial pneumonia , and a significant reduction in hospital costs  when the tracheostomy is performed within 1 week of their injuries. Similar benefits have been reported in patients with head trauma and poor Glasgow Coma Score , acute spine trauma , and thermal injury  if a tracheostomy is performed within a week after the injury. Also, patients with facial injuries may require early tracheostomy to allow or facilitate facial fracture surgery, fixation, and immobilization. When time is short, the patient is uncooperative, anatomy is distorted, and the aforementioned requirements are not met, then tracheostomy can be very hazardous. Emergency tracheostomy comprises significant risks to nearby neurovascular structures, particularly in small children in whom the trachea is small and not well defined. The risk of complications from emergency tracheostomy is two to five times higher than for elective tracheostomy [27,28]. Nonetheless, there are occasional indications for emergency tracheostomy , including transected trachea; anterior neck trauma with crushed larynx ; severe facial trauma; acute laryngeal obstruction or near-impending obstruction; and pediatric (younger than 12 years) patients requiring an emergency surgical airway in whom a cricothyrotomy is generally not advised. In emergency situations, when there is inadequate time or personnel to perform an emergency tracheostomy, a cricothyrotomy may be a more efficient and expedient manner to provide an airway. Cricothyrotomy Although initially condemned because of a high rate of complications, cricothyrotomy may have some potential advantages over tracheostomy. These include technical simplicity; speed of performance; low complication rate ; suitability as a bedside procedure; usefulness for isolation of the airway for median sternotomy and radical neck dissection ; lack of need to hyperextend the neck; and formation of a smaller scar. Also, because cricothyrotomy results in less encroachment on the mediastinum, there is less chance of esophageal injury and virtually no chance of pneumothorax or tracheal arterial fistula . Despite these considerations, many authorities currently recommend that cricothyrotomy be used as an elective long-term method of airway access only in highly selected patients . Use of cricothyrotomy in the emergency setting, particularly for managing trauma, is not controversial [35–37]. Emergency cricothyrotomy is useful because it requires a small number of instruments and less training than tracheostomy, and can be performed quickly as indicated as a means of controlling the airway in an emergency when oral or nasotracheal intubation is nonsuccessful or contraindicated. The cricothyroid membrane is higher in the neck than the tracheal rings and therefore closer to the surface and more accessible. In emergency situations, translaryngeal intubations fail because of massive oral or nasal hemorrhage or regurgitation; structural deformities of the upper airway; muscle spasm and clenched teeth; and obstruction by foreign body through the upper airway . Cricothyrotomy finds its greatest use in trauma management, axial or suspected cervical spine injury, alone or in combination with severe facial trauma, where nasotracheal and orotracheal intubation is both difficult and hazardous. Use and Contraindications Cricothyrotomy should not be used to manage airway obstruction that occurred immediately after endotracheal extubation because the obstruction may be found below the larynx ; likewise, with primary laryngeal trauma or diseases such as a tumor or an infection, cricothyrotomy may prove to be useless. It is contraindicated in infants and children younger than 10 to 12 years under all circumstances because stenosis and even transection are possible . In this age group, percutaneous needle catheter transtracheal ventilation may be a temporizing procedure until the tracheostomy can be performed. Anatomy the cricothyroid space is no larger than 7 to 9 mm in its vertical dimension, smaller than the outside diameter of most tracheostomy tubes (outside diameter 10 mm). The cricothyroid artery runs across the midline in the upper portion, and the membrane is vertically in the midline. The cricothyroid membrane is approximately 2 to 3 cm below the laryngeal prominence and can be identified as an indentation immediately below the thyroid cartilage. This major complication occurs at the tracheostomy or cricothyrotomy site, but not at the cuff site . Necrosis of cartilage due to iatrogenic injury to the cricoid cartilage or pressure from the tube on the cartilage may play a role . Possible reasons that subglottic stenoses may occur more commonly with cricothyrotomy than with tracheostomy are as follows: the larynx is the narrowest part of the laryngotracheal airway; subglottic tissues, especially in children, are intolerant of contact; and division of the cricothyroid membrane and cricoid cartilage destroy the only complete rings supporting the airway. Furthermore, the range of tube sizes is limited because of the rigidity of the surrounding structures (cricoid and thyroid cartilages), and the curvature of the tracheostomy tube at this level may obstruct the airway because of posterior membrane impingement . Prior laryngotracheal injury, as with prolonged translaryngeal intubation, is a major risk factor for the development of subglottic stenosis after cricothyrotomy . The association of cricothyrotomy with these possible complications leads most authorities to consider replacing a cricothyrotomy within 48 to 72 hours with a standard tracheostomy procedure. There are two major techniques for tracheostomy, open and percutaneous, with various modifications of each. The different surgical tracheostomy techniques are well described in the references for this chapter [3,40]. This area is prepped and draped, and prophylactic antibiotics are administered at the discretion of the surgeon. A vertical or horizontal incision may be used; however, a horizontal incision will provide a better cosmetic result.