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Damage to the tissues in the airways or lung parenchyma does not always occur when smoke is inhaled gastritis symptoms home remedies purchase discount clarithromycin line. Inhalation injury will depend on the amount of exposure gastritis y probioticos buy clarithromycin with american express, the heat and composition of the smoke gastritis diet áîëüøèå cheap clarithromycin master card, and probably the individual susceptibility of the victim. Cutaneous burns over the face and singed facial or nasal hair are evidence of exposure to intense heat near the airways. It also means that the victim was unable to escape exposure or injury, since the face is generally protected from TABLE 3 Physical examination findings associated with inhalation injury Respiratory distress Soot over face or in sputum Burns over face or neck Singed facial or nasal hair Oropharyngeal burns Tachypnea Hoarseness Strider Drooling Signs of airway obstruction Inhalation Injury 63 heat by vigorous avoidance behavior. Patients with facial burns should be ob- served closely for signs and symptoms of upper airway obstruction by edema. These patients should also have their oropharynx examined for mucosal burns. The patient may also show preference for the upright position for breathing. Hypoxia can cause altered mental status, confusion, or a decreased level of consciousness. Extensive full-thickness burns to the chest, especially circumferential injuries, may result in a restrictive ventilatory defect. More superficial thoracic burns can cause a similar defect as thoracic compliance is decreased slowly by edema that develops during resuscita- tion with fluids. Dyspnea, hoarseness, and coughing are often present initially in burn pa- tients but often resolve spontaneously. Stridor should be differentiated from hoarseness as a more ominous sign. High-pitched inspiratory noise over the upper airway is characteristic of critical narrowing of the airway. In the context of fluid resuscitation for burn injuries, this can be rapidly progressive and demands immediate evaluation and probably intervention as well. Other signs of airway obstruction include use of accessory respiratory muscles, sternal and suprasternal retractions, and paradoxical thoracoabdominal movement. Evaluation of the impact of an inhalation injury must take into account the presence of associated injuries. The combination of full-thickness burns with inhalation injury requires a larger volume of fluid for resuscitation than for the burns alone. Underresuscitation as well as overresuscitation of cutaneous burns can exacerbate the effects of an inhalation injury. The ability of a patient to compensate for an inhalation injury is diminished by injuries that make breathing difficult (e. None of the above observations from the history and physical examination can be considered 100% sensitive and specific for inhalation injury. The value of these clinical indicators increases when multiple risk factors coexist. It has been stated that the diagnosis of inhalation injury becomes easier with the passage of time. However, morbidity is minimized by early diagnosis and treatment of inhalation injury. Diagnostic Studies History and physical examination will identify patients at risk for inhalation injury as well as those who urgently need intubation and mechanical ventilation.
Central hyperventilation may also occur late in uncal herniation FIGURE 2–5 gastritis diet tips purchase clarithromycin 250 mg on-line. Temporal Lobe—Tentorial (Uncal) Herniation 66 TRAUMATIC BRAIN INJURY Heterotopic Ossification (HO) HO is the formation of mature lamellar bone in soft tissue Common in TBI gastritis diet çàéöåâ buy clarithromycin 250 mg visa, with an incidence of 11%–76% (incidence of clinically significant cases is 10%–20%) Risk factors: Prolonged coma (> 2 weeks) – Immobility – Limb spasticity/↑ tone (in the involved extremity) – Associated long-bone fracture – Pressure ulcers – Edema Period of greater risk to develop HO: 3 to 4 months post injury Signs/Symptoms – Most common: pain and ↓ range of motion (ROM) – Also: local swelling gastritis diet ôàöåáîîê generic clarithromycin 250mg amex, erythema, warmth joint, muscle guarding, low-grade fever In addition to pain and ↓ ROM, complications of HO include bony ankylosis, peripheral nerve compression, vascular compression, and lymphedema Joints most commonly involved: 1. Knees Differential Dx: DVT, tumor, septic joint, hematoma, cellulitis, and fracture Diagnostic Tests/Labs Serum Alkaline Phosphatase (SAP) SAP elevation may be the earliest and least expensive method of detection of HO It has poor specificity (may be elevated for multiple reasons, such as fractures, hepatic dys- function, etc. Useful to confirm maturity of HO Prophylaxis ROM exercises Control of muscle tone Non Steroidal Anti-inflammatory Drugs (NSAIDs) Radiation—used perioperatively to inhibit HO in total hip replacement patients; concerns about ↑ risk of neoplasia limit its use in younger patient populations (e. Also, as radiation is used prophylactically to prevent HO formation of a particular joint, to use it in TBI patients would require essentially irradiation of the whole body (as HO can develop practically at any joint), which is not practical TRAUMATIC BRAIN INJURY 67 Treatment Diphosphonates and NSAIDs (particularly indomethacin) have been used on patients to arrest early HO and to prevent postop recurrence, but their efficacy has not been clearly proven (TBI population) ROM exercises—used prophylactically to prevent HO and also used as a treatment for developing HO (to prevent ankylosis) Surgery—surgical removal of HO indicated only if ↑ in function is a goal (to ↑ hygiene, sitting, etc. IVC filter used when anticoagulation is contraindicated Posttraumatic Epilepsy/Posttraumatic Seizures (PTS) Posttraumatic epilepsy is classified as: 1. Partial (simple, if consciousness is maintained, or complex, if not) The majority of PTS are of the partial type Posttraumatic seizures are further classified as: Immediate PTS—occur within the first 24 hours post injury Early PTS—occur within the first week (24 hours to 7 days) Late PTS—occur after the first week – Immediate PTS has better prognosis than early epilepsy; early PTS associated with increased risk of late PTS Incidence Varies greatly according to the severity of the injury, the time since the injury, and the pres- ence of risk factors (see below) 5% of hospitalized TBI patients (overall, closed-head injury) have late PTS 4%–5% of hospitalized TBI patients have one or more seizures in the first week after the injury (early PTS) (Rosenthal et al. A group of 4541 patients with TBI {characterized by loss of consciousness (LOC), posttraumatic amnesia (PTA), SDH or skull fracture}, were divided into three categories: Mild TBI—LOC or amnesia < 30 minutes Moderate TBI—LOC for 30 minutes to 24 hours or skull fractures Severe TBI—LOC or amnesia > 24 hours, SDH or brain contusion Incidence of seizures in the different categories: Mild TBI—1. There is no proof of change in outcome with prophy- lactic use of phenytoin (Temkin et al. TABLE 2–10 Anticonvulsant Medications: Uses and Adverse Reactions Medication Uses Adverse Reactions Carbamazepine Partial seizures Acute: stupor or coma, hyperirritability, Tonic-clonic; generalized convulsions, respiratory depression seizures Chronic: drowsiness, vertigo, ataxia, diplopia, Stabilization of agitation blurred vision, nausea, vomiting, aplastic anemia, and psychotic behavior agranulocytosis, hypersensitivity reactions Bipolar affective disorder (dermatitis, eosinophilia, splenomegaly, Neuralgia lymphadenopathy), transient mild leukopenia, transient thrombocytopenia, water retention with decreased serum osmolality and sodium, transient elevation of hepatic enzymes Gabapentin Partial seizures Somnolence, dizziness, ataxia, fatigue Lamotrigine Partial seizures Dizziness, ataxia, blurred or double vision, Tonic-clonic; generalized nausea, vomiting, rash, Stevens-Johnson seizures syndrome, disseminated intravascular coagulation Phenobarbital Partial seizures Sedation, irritability, and hyperactivity in Tonic-clonic; generalized children, agitation, confusion, rash, exfoliative seizures dermatitis, hypothrombinemia with hemorrhage in newborns whose mothers took phenobarbital, megaloblastic anemia, osteomalacia Nystagmus and ataxia at toxic doses Phenytoin Partial seizures Intravenous administration: cardiac Tonic-clonic; generalized arrhythmias, hypotension, CNS depression seizures Oral administration: disorders of the cerebellar Neuralgia and vestibular systems (such as nystagmus, ataxia, and vertigo), cerebellar atrophy, blurred vision, mydriasis, diplopia, ophthalmoplegia, behavioral changes (such as hyperactivity, confusion, dullness, drowsiness, and hallucination), increased seizure frequency, gastrointestinal symptoms, gingival hyperplasia, osteomalacia, megaloblastic anemia, hirsutism, transient liver enzyme elevation, decreased antidiuretic hormone secretion leading to hypernatremia, hyperglycemia, glycosuria, hypocalcemia, Stevens-Johnson syndrome, systemic lupus erythematosus, neutropenia, leukopenia, red cell aplasia, agranulocytosis, thrombocytopenia, lymphadenopathy, hypothrombinemia in newborns whose mothers received phenytoin, reactions indicative of drug allergy (skin, bone marrow, liver function) Valproic Acid Partial seizures Transient gastrointestinal symptoms such as Tonic-clonic; generalized anorexia, nausea, and vomiting; increased seizures appetite; sedation; ataxia; tremor; rash; alopecia; Myoclonic seizures hepatic enzyme elevation, fulminant hepatitis Absence seizures (rare, but fatal); acute pancreatitis; Stabilization of agitation hyperammoniemia and psychotic behavior From Rosenthal M, Griffith ER, Kreutzer JS, Pentland B. Rehabilitation of the Adult and Child with Traumatic Brain Injury 3rd ed. Their superiority over phenytoin has been debated (differences among these three agents are probably minimal); carbamazepine may be as sedating as phenytoin. Animal and clinical (extrapolated from strokes) studies suggest that phenytoin may impede recovery from brain injury (Dikmen, 1991) Second generation anticonvulsants, such as gabapentin and lamotrigine, may also be used for treatment of PTS as adjuvant agents (not approved yet for monotherapy). These agents appear to have fewer cognitive side effects, but are still under investigation in the TBI population. Anticonvulsant Medications: Common Drug Interactions Medication Drug Interaction Carbamazepine Increased metabolism of carbamazepine (decreased levels) with phenobarbital, phenytoin, and valproic acid Enhances metabolism of phenobarbital Enhances metabolism of primidone into phenobarbital Reduces concentration and effectiveness of haloperidol Carbamazepine metabolism inhibited by propoxyphene and erythromycin Lamotrigine When used concurrently with carbamazepine, may increase levels of 10,11 –epoxide (an active metabolic of carbamazepine) Half-life of lamotrigine is reduced to 15 hours when used concurrently with carbamazepine, phenobarbital, or primidone Reduces valproic acid concentration Phenobarbital Increased levels (as much as 40%) of phenobarbital when valproic acid administered concurrently Phenobarbital levels may be increased when concurrently administering phenytoin Phenobarbital has a variable reaction with phenytoin levels Phenytoin Phenytoin levels may increase with concurrent use of chloramphenicol, cimetidine, dicumarol, disulfiram, isoniazid, and sulfonamides Free phenytoin levels may increase with concurrent use of valproic acid and phenylbutazone Decreased total levels of phenytoin may occur with sulfisoxazole, salicylates, and tolbutamide Decreased phenytoin levels with concurrent use of carbamazepine Decreased carbamazepine levels with concurrent use of phenytoin Increased or decreased levels of phenytoin when concurrently administered with phenobarbital When concurrently used with theophylline, phenytoin levels may be lowered and theophylline metabolized more rapidly May decrease effectiveness of oral contraceptives Enhances metabolism of corticosteroids Valproic Acid Increases level of phenobarbital Inhibits metabolism of phenytoin Rare development of absence status epilepticus associated with concurrent use of clonazepam (Reprinted with permission from Rosenthal et al. It has been suggested to withdraw anticonvulsant medications after a seizure-free interval of 3 months to 6 months up to 1–2 years. Agitation may be con- trolled with alterations in environment and staff or family behavior Floor beds can eliminate need for restraints Use physical restraints only if patient is a danger to self or others; should be applied only to minimal degree and not as a substitute for floor bed or one-to-one or other environ- mental interventions TABLE 2–12. Reduce the level of stimulation in the environment Place patient in quiet private room Remove noxious stimuli if possible, tubes, catheters, restraints, traction Limit unnecessary sounds, TV, radio, background conversations Limit number of visitors Staff to behave in a calm and reassuring manner Limit number and length of therapy sessions Provide therapies in patient room 2. Protect patient from harming self or others Place patient in a floor bed with padded side panels (Craig bed) Assign 1:1 or 1:2 sitter to observe patient and ensure safety Avoid taking patient off unit Place patient in locked ward 3. Reduce patient’s cognitive confusion One person speaking to patient at a time Maintain staff to work with patient Minimize contact with unfamiliar staff Communicate to patient briefly and simple, one idea at a time 4. Tolerate restlessness when possible Allow patient to thrash about in floor bed Allow patient to pace around unit with 1:1 supervision Allow confused patient to be verbally inappropriate (Reprinted with permission from Braddom RL. The use of a floor bed with one-to-one supervision and with the use of mitts and a helmet (if necessary) often eliminates the need for restraints. If nerve is completely involved or transected, patient will develop complete blindness (pupil dilated, unreactive to direct light but reactive to light stimulus to the opposite eye (consensual light reflex) Endocrine Complications Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) Water retention resulting from excessive antidiuretic hormone (ADH) secretion from the neurohypophysis secondary to multiple causes including head trauma In SIADH, ADH excess considered to be inappropriate because it occurs in the presence of plasma hypo-osmolality In SIADH, Na+ excretion in the urine is maintained by hypervolemia, suppression of the renin-angiotensin-aldosterone system, and ↑ in the plasma concentration atrial natriuretic peptide (usually > 20 mmol/L) Common Causes of SIADH CNS Diseases Malignancy – Thrombotic or hemorrhagic events – CA of the lung (especially small cell CA) – Infection – GI malignancy (e. Comparison of SIADH, CSW and DI SIADH DI CSW syndrome Serum ADH (rarely done ↑ (inappropriately (appropriately as routine lab work) elevated) elevated) Diagnostic Labs Serum Na+ Serum osmolality Extracellular volume Normal (isovolemic) Normal (isovolemic) Reduced (hypovolemic) Urine osmolality and SG ↑ (concentrated urine ↓ Normal with osmolality usually > 300 mmol/kg) Spasticity Disorders of motor tone (e. This condition has been termed postconcussive syndrome (PCS) In a recent study, 14 mild TBI patients with unusually persistent deficits evaluated with single photon emission computed tomography (SPECT) showed significant anterior mesial temporal (lobe) hypoperfusion and less striking dominant (left) orbitofrontal abnormalities Memory and learning deficits have been associated with lesions at the hippocampus and related structures in the medial temporal lobes or with injuries to structures that control attention, concentration, and information processing in the frontal and temporal lobe Pharmacologic intervention may be used including antidepressants and psychostimulants Concussion/Sports Related Head Injuries Classification of concussion is controversial The most widely used grading systems for concussion/mild head injury are the Colorado and the Cantu guidelines TABLE 2–14.
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