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1、 CHAPTER 23SURGICAL CRITICAL CARECharles A. Adams, Jr., Andrew Stephen, and William G. Cioffimetabolic conditions, whereas exogenous causes can include medications, environmental settings, and toxins. Any unex- plained changes in a surgical patients level of consciousness or sensorium should be work

2、ed up thoroughly. Ascribing such changes to ICU psychosis should be considered strictly a diag- nosis of exclusion.1 The term altered mental status is nonspecific and more descriptive definitions were offered by Plum and Posner almost 30 years ago in their text on stupor and coma and still apply tod

3、ay. The term confusion encompasses bewilderment, difficulty following commands, disturbed memory, and drowsi- ness or nighttime agitation, whereas delirium is a floridly abnormal mental state characterized by disorientation, fear, irritability, misperception of sensory stimuli and, often, visual hal

4、lucinations.The presence of delirium can have far-reaching conse- quences and is associated with increased hospital length of stay and mortality.2 Obtundation is defined as mental blunting asso- ciated with slowed psychological responses to stimulation. Stupor is described as a condition of deep sle

5、ep or behaviorally similar unresponsiveness in which the patient can be aroused only by vigorous and repeated stimuli. Coma is a state of unarousable psychological unresponsiveness in which the subject lies with eyes closed and shows no psychologically understand- able response to external stimuli o

6、r inner need. A vegetative state is a state of wakefulness but with apparent complete lack of cognitive function. Death in the presence of cardiopulmonary function (brain death) refers to the absence of function of the brain and brainstem; there are specific criteria for this, but the absence of cer

7、ebral function is paramount. Cortical nonfunction must be accompanied by the loss of reflexes to pupillary light and corneal stimulation, loss of the vestibulo-ocular and oropha- ryngeal reflexes, and apnea in the presence of adequate stimula- tion (PaCO2 > 60 mm Hg for 30 seconds). Generally, tw

8、o clinical examinations must be documented, separated by a defined time interval (e.g., 6 hours) and confirmed by independent physi- cians; however, there is no nationally accepted definition of brain death. It is important that there be a reason or physiologic insult sufficient to cause death and t

9、here are no complicating or reversible conditions (e.g., recent administration of sedative or anesthetic agents, hypothermia, hypo- or hyperglycemia, or severe hypo- or hypernatremia, or other significant metabolic derangements) that could interfere with brain death determina- tion. If such complica

10、ting conditions preclude the completion of a clinical examination, additional tests are required, including563The goal of surgical therapy, elective or urgent, is to enable patients to return to their preoperative state of health and func- tional status. However, some patients have surgical processe

11、s or injuries that are so severe that they would either not survive or would suffer significant long-term morbidity without specialized supportive care. These types of patients require multisystem surgical critical care delivered by specialized teams of trained health care providers in an intensive

12、care unit (ICU). Although many of these ICUs are closed units or structured so that patient management decisions are made solely by the critical care team, it is important that surgeons remain current and acquainted with the ever-changing field of surgical critical care so that they can remain a vit

13、al part of the patients health care team, espe- cially in systems or institutions in which critical care of surgical patients is being delivered by nonsurgical specialists. In this chapter, we will approach the vast topic of surgical critical care in a system-based fashion and highlight recent devel

14、opments and concepts.CENTRAL NERVOUS SYSTEMNeurologic DysfunctionThe central nervous system (CNS) is the most complex organ system in the body and is vulnerable to disturbances by a host of conditions and factors. The causes of an altered consciousness are so broad that a clouded sensorium is the no

15、rm in the ICU rather than the exception. This list of conscious-altering causes includes endogenous and exogenous factors. Some endoge- nous causes include sepsis, CNS infections, hypoxic-ischemic encephalopathy, tumors, trauma, electrolyte derangements, andcentral nervous system cardiovascular syst

16、em respiratory system gastrointestinal system acute kidney injury hepatic dysfunction endocrine system hematologic systemsepsis and multiple organ failure564 SECTION III TRAUMA AND CRITICAL CAREprovocative tests (e.g., apnea test). Electroencephalography, radioisotope brain scanning, transcranial Do

17、ppler ultrasonogra- phy, and cerebral arteriography with documentation of absent cortical flow are all helpful in defining brain death but this diagnosis must conform to the criteria set forth by each state government and the hospitals contained within.When there is an alteration in a patients neuro

18、logic status, an assessment should be done thoroughly and rapidly, with initial management and corrective measures instituted concur- rently to minimize irreversible CNS damage. The patients level of consciousness may be described as alert, responsive to verbal stimuli, responsive to painful stimuli

19、, or unresponsive. Acute loss of consciousness that occurs in a period of seconds to minutes is consistent with a cerebrovascular accident or head trauma. A subacute course that occurs in many minutes to hours may suggest intoxication, infection, or a metabolic disturbance, whereas a more prolonged

20、course of neurologic decline may suggest a CNS tumor. The pupillary examination can be particu- larly informative. Damage to the midbrain affects the reticular activating system, and thus consciousness, as well as pupil reac- tivity, whereas metabolic disease may produce coma but usually leaves the

21、light reflex intact. Small reactive pupils are the hall- mark of drug intoxication (particularly opiate) and metabolic disease, whereas large unreactive pupils may be associated with anticholinergic drugs, glutethimide, anoxia, or intracranial hypertension. A unilateral fixed and dilated pupil sugge

22、sts third nerve dysfunction or uncal herniation. In the absence of pur- poseful eye movements, spontaneous roving eye movements imply intact cortical control of the brainstem. If no spontaneous eye movement is found, the vestibulo-ocular reflex (dolls eye maneuver) should be tested after excluding a

23、 cervical cord or spine lesion. This reflex is tested by turning the head rapidly from midline to one side. Contralateral conjugate eye move- ment, keeping the eyes seemingly fixed on a point in space, suggests an intact brainstem. The head should be turned in the opposite direction to check for sym

24、metry. Failure of this reflex in either direction implies brainstem dysfunction. If this maneu- ver cannot be done, the vestibulo-ocular reflex may be assessed by a cold caloric testing technique instead. This is done by ele- vating the head to 30 degrees and rapidly instilling 50 mL of ice water in

25、to the external auditory canal, which results in reflex slow eye movement toward the stimulus. In an intact brain, the frontal eye fields attempt to override this stimulus, producing rapid saccades away from the stimulus (nystagmus). Conversely, if there is cortical damage, the eyes will maintain a

26、fixed devia- tion, which implies a hemispheric lesion on the side toward which the eyes deviate. Assessment of motor function helps identify the location and severity of deficits. The motor compo- nent of the Glasgow Coma Scale is the most predictive portion of the scale following head trauma. Asymm

27、etry of motor func- tion suggests a focal cerebral lesion contralateral to the deficit. Decorticate (flexion of arms and extension of legs) and decere- brate (extension of both arms and legs) posturing are very poor prognostic signs.Although it is important for staff physicians and surgicalsimultane

28、ously and thus are able to perform these evaluations on a frequent basis. The confusion assessment method for iden- tifying ICU delirium (CAM-ICU) is a rapid, objective measur- ing tool to determine the presence of delirium and can be performed serially with relative ease.2 CAM-ICU is straightfor- w

29、ard and addresses whether there is an acute or fluctuating onset of a patients mental status change or delirium, general inatten- tion, disorganized thought, or altered level of consciousness. Themerequired for each CAM-ICU assessment is less than1 minute and can be performed by any trained health c

30、are pro- vider (e.g., physician, nurse, respiratory therapist); its reliabilityand accuracy has been validated in prospective cohort studies weighed against the standard of evaluations of delirium experts using criteria from the Diagnostic and Statistical Manual of Mental Disorders. The importance o

31、f a tool such as CAM-ICU lies in its ability to identify delirium quickly, accurately, and easily so that appropriate drug therapy may be instituted.Laboratory studies also can help identify metabolic derange- ments such as hypothyroidism, electrolyte abnormalities, infections, and toxic ingestions.

32、 Urine toxicology screening is mandatory because drug intoxication is one of the most common initial causes of coma of unknown cause. Arterial blood gas (ABG) analysis should be performed to rule out hypoxia, hyper- carbia, or acidosis as a cause of an altered mental state. Com- puted tomography (CT

33、) is indicated for any patient with coma and focal neurologic findings or in patients with a depressed level of consciousness that prevents an adequate physical exami- nation from being carried out. A lumbar puncture should be performed on any patient for whom the cause of coma is still unknown, esp

34、ecially patients in whom meningitis, encephalitis, or occult subarachnoid hemorrhage is suspected. In the post head injury or neurosurgical postoperative patient, clinical dete- rioration in the absence of a new structural lesion (i.e., CT scan finding) coupled with signs of infection (e.g., fever,

35、leukocytosis) may be a sign of CNS infection and a lumbar puncture is warranted.Initial management begins with assurance of a patent airway and adequate breathing and circulation (the ABCs, as taught by the Advance Trauma Life Support program). Coma- tose patients should be intubated for airway prot

36、ection; however, stability of the cervical spine must be ensured in trauma patients. If there is a possibility of increased intracranial pressure (ICP), lidocaine (1.5 mg/kg) or thiopental (3 to 5 mg/kg) should be administered to blunt sudden rises in ICP associated with intu- bation. Hypotension sh

37、ould be corrected promptly and aggres- sively with fluids and/or vasopressors to maintain an adequate cerebral perfusion pressure (CPP) of at least 55 to 60 mm Hg. CPP is calculated as the difference between a patients mean arterial pressure (MAP) and intracranial pressure (CPP = MAP ICP). A dose of

38、 50 mL of 50% dextrose should be given immediately to any patient with coma of unknown cause . This will produce no detrimental effect on any causes of coma except Wer es encephalopathy (see later) and will correct the under- lying problem if it is secondary to hypoglycemia. Even in those patients w

39、ith hyperglycemia producing the coma, a marginal increase in the glucose concentration will not adversely affect the patient; however, the effects of any significant period of marked hypoglycemia may result in irreversible neurologic damage. In alcoholic patients or others with poor general nutri- t

40、ion, thiamine (1 mg/kg) should be administered before glucose. This may avoid acute Wernick encephalopathy (confusion,housenel to become comfortable and proficient with theneurologic examination of critically ill and ventilated patients, it is tremendously beneficial when nurses provide frequent obj

41、ective evaluations and can relay any significant changes to thesurgical team, especially regarding states of delirium or confu- sion. ICU nurses generally care for limited numbers of patientsSURgICAL CRITICAL CARE ChapTEr 23 565ataxia, ophthalmoplegia) and its associated necrosis of midline gray mat

42、ter.Narcotic overdose is a common cause of coma and is marked by shallow respirations, small reactive pupils, and hypo- tension. Naloxone (Narcan; 0.4 to 2 mg) is an opioid antagonist and should be given to patients with suspected opiate-induced coma. Flumazenil (0.2 mg) may be administered for susp

43、ected benzodiazepine intoxication, but care should be exercised in patients taking benzodiazepines on a chronic basis or suspected mixed ingestions because other agents may lower the seizure threshold, leading to severe seizures following flumazenil admin- istration. Activated charcoal (25 to 50 mg)

44、 should be given for the ingestion of most drugs and toxins, but its effectiveness diminishes as the interval from ingestion to administration increases. Empirical antibiotic therapy directed at suspected demographic-associated pathogens is warranted if bacterial men- ingitis is suspected.If increas

45、ed ICP is assumed to be the cause of coma, treat- ment should be initiated immediately with elevation of the head of the bed to 30 to 45 degrees. Hyperventilation is effective in lowering the ICP, but prolonged or extreme hyperventilation can lead to cerebral vasoconstriction and detrimental regiona

46、l isch- emia. Also, it is likely that the vasoconstricting effects of hyper- ventilation to decrease ICP are lost within 24 hours as the cerebral circulation reflexively normalizes with the new lower PaCO2. Thus, a target PaCO2 of 35 to 40 mmHg is considered optimal and there is unlikely benefit of

47、lower levels of PaCO2. Vasogenic cerebral edema leads to increased ICP according to the Monro-Kellie hypothesis, which states that the pressure inside the head must rise if any intracranial component increases (e.g., blood, brain, cerebrospinal fluid) because the cranial vault is a rigid, nonexpansi

48、ve structure. Accordingly, the osmotic diuretic mannitol (0.5 to 1 g/kg) should be administered; this may be repeated every 4 to 6 hours as long as the serum sodium level and osmolarity remain less than 155 and 320 mmol/liter, respectively. However, mannitol should be avoided in situations in which

49、such diuresis may compromise hemodynamics by decreasing the MAP and, in turn, the patients CPP. Hypertonic saline 3% and, more recently, saline 23.4% have also been shown to be effective and safe therapies for managing intracra- nial hypertension via osmotic mechanisms without compromis- ing the MAP

50、 as the way diuretics tend to do. Currently, most studies comparing hypertonic saline to mannitol are retrospec- tive; thus, more randomized prospective investigation is war- ranted. Other factors involved in managing ICP include adequate sedation and suppression of fever and seizures. If the patien

51、t has refractory intracranial hypertension, second-tier therapies should be used, including ventriculostomy drainage, neuromuscular blockade, vasopressors to increase CPP, barbiturate coma, and decompressive craniectomy.Seizure activity is often the first sign of a CNS complica-tion. Because most se

52、izures terminate rapidly, the most impor- tant initial intervention is protecting the patient from harm, most notably failure to protect the airway and self-injury. The cause of the seizures should be investigated and treated. CT scanning or magnetic resonance imaging (MRI) of the brain is indicated

53、 for new-onset seizures, and electroencephalograms should be obtained to exclude status epilepticus in patients who have persistent or recurrent seizures or who do not awaken after seizure activity. Status epilepticus should be treated with benzodiazepines, such as lorazepam (0.1 mg/kg), followed by

54、phenytoin (1 g). If this regimen is unsuccessful in breaking the seizure activity, second-tier therapies should be administered, such as high-dose benzodiazepines, barbiturates, or propofol. The major systemic complications of seizures are rhabdomyoly- sis, hyperthermia, and cerebral edema.Analgesia

55、, Sedation, and Neuromuscular Blockade Pain and anxiety are common in ICU patients. Pain may be caused by an underlying disease state, trauma, invasive proce- dures, or surgical wounds. Pain is exacerbated by nursing inter- ventions, invasive monitoring, therapeutic devices, immobility, and mechanic

56、al ventilation. Unrelieved pain can provoke a sym- pathetic stress response, as well as contribute to agitation and metabolic stress. Unfortunately, the severity of pain is often underappreciated in the ICU and consequently may be treated suboptimally. A universal goal for physicians is ensuring an

57、optimal level of comfort and safety for all patients.Pain Assessment and ManagementPerception of pain is influenced by prior experiences, negative expectations, and the cognitive capacity of the patient. The patient and family should be advised of the potential for pain and strategies to communicate

58、 pain. Patient self-reporting is the gold standard for the assessment of pain and the adequacy of analgesia. Pain assessment tools such as the visual analogue scale or numeric rating scale are most useful. In noncommunicative patients, assessment of behavioral (e.g., movements, facial expressions, p

59、osturing) and physiologic (e.g., heart rate, blood pressure, respiratory rate) indicators are necessary. It is para- mount that the surgical staff and house officers communicate effectively with ICU nurses because their frequent assessments of pain consistently seem to lead to earlier and timelier admin- istration of pain medications. Nurse-driven protocols for pain assessment and management have been shown to reduce ventila- tor days and ICU length of stay while at the same time pro