Max S. Topp, M.D.

• Director
• Internal Medicine II
• University Medical Center II
• W?rzburg, Germany

Glucocorticoids are beneficial gastritis diet 8i discount 20 mg bentyl free shipping, and because the necrotic lesion has mass effect treating gastritis with diet order 20mg bentyl free shipping, surgical extirpation is often useful follicular gastritis definition cheap 20mg bentyl with visa. Late delayed damage to the spinal cord results in a progressive myelopathy that may be asymmetric in onset; typically gastritis diet 8 month purchase discount bentyl line, numbness and weakness ascend and progress to symmetric paraplegia chronic gastritis with intestinal metaplasia generic 20mg bentyl with amex. This disorder is secondary to necrosis of the white matter and usually occurs with doses 5 gastritis symptoms deutsch order 20mg bentyl,000 cGy given over 5 weeks by conventional fractionation. Visual loss can result from radiation-induced optic neuropathy, retinopathy, glaucoma, cataract formation, and dry-eye syndrome. Hearing loss is caused by otitis media (acute or early delayed effect) or by sensorineural damage (late delayed effect). Hormonal deficiencies occur as a result of hypothalamic and pituitary dysfunction after cranial irradiation. The most common deficiency involves growth hormone, but thyroid, adrenal, and gonadal dysfunctions also occur. Acute and early delayed reactions are self-limited but often respond to treatment with steroids. Late delayed reactions, which are usually caused by neuronal and glial injury, do not recover with treatment; however, steroids can reduce swelling and symptoms in patients with radionecrosis. If small, the radionecrosis will eventually resolve on its own, but if the involved region is large, resection of the dead tissue may be necessary. Radiation-induced tumors tend to occur decades after irradiation and include meningiomas, nerve sheath tumors, astrocytomas, and sarcomas; these tumors are usually malignant. Chemotherapeutic agents may be toxic to the entire nervous system or cause more limited neurotoxicity, affecting only the central or peripheral nervous system. Encephalopathy (insomnia, agitation, drowsiness, depression, confusion, headache) usually develops acutely after administration of the offending agent. Responsible agents include methotrexate, cytarabine, procarbazine, mitotane, l-asparaginase, ifosfamide, cisplatin, vincristine, 5-fluorouracil, tamoxifen, nitrosourea, etoposide, interferon-a, pentostatin, tegafur, levamisole, and, rarely, hexamethylmelamine, fludarabine, and 5-azacitidine. Cerebellar syndrome (ataxia, nausea and vomiting, nystagmus) can be seen after the use of cytarabine, procarbazine, fluorouracil, and the nitrosoureas. Seizures may occur after cisplatin, hydroxyurea, l-asparaginase, ifosfamide, procarbazine, and rarely vincristine. Peripheral neuropathy (paresthesias, loss of deep tendon reflexes, distal extremity weakness) is a common neurologic complication of chemotherapy. The neuropathy is cumulative and is at least partially (if not completely) reversible with discontinuation of the offending agent. Other drugs that can cause neuropathy include bortezomib (Velcade), docetaxel (Taxotere), paclitaxel (Taxol), thalidomide, vindesine, vinblastine, procarbazine, suramin, hexamethylmelamine, etoposide, and teniposide. Cranial neuropathy (loss of hearing, vision, taste) may develop from the use of cisplatin, vincristine, and the nitrosoureas. Myelopathy (quadriparesis, paraparesis, bowel and bladder dysfunction) is a rare complication of intrathecal chemotherapy, including methotrexate and cytarabine. Myelopathy has been reported only after drug administration via lumbar puncture, not through an intraventricular (Ommaya) reservoir. The combination of cranial irradiation and chemotherapy, particularly with methotrexate, nitrosoureas, or cytarabine, can have a synergistic toxic effect on normal brain structures. This can lead to permanent damage, often affecting the white matter and causing a leukoencephalopathy that produces a progressive dementing process. No known treatment exists, but some patients temporarily benefit from a ventriculoperitoneal shunt. Nonbacterial thrombotic endocarditis, seen especially with adenocarcinoma of the lung and gastrointestinal tract, is probably the most common cause of cerebral infarction in patients with carcinoma, although it is difficult to diagnose. Diagnosis of the valvular lesions is best established by transesophageal echocardiogram. Thrombosis can cause strokes (arterial) as well as occlusion of the superior sagittal sinus (venous). The latter syndrome presents with headache, obtundation, and sometimes bilateral venous infarcts that may be hemorrhagic. Chemotherapy, especially with l-asparaginase, which causes venous sinus thrombosis. Vasculitis, usually as a complication of herpes zoster infection or seen in patients with Hodgkin disease. Hemorrhages are more common in patients with leukemia but can occur in those with solid tumors as well. Hematogenous dissemination to the eye also complicates acute leukemia, melanoma, sarcoma, and carcinomas of the lung, bladder, and prostate. Fundal hemorrhages, leukemic infiltrates, or masses may be evident on ophthalmoscopy. Embolic retinal artery occlusion is most commonly caused by atherosclerosis but may rarely be seen with atrial myxoma, nonbacterial thrombotic endocarditis, and cryoglobulinemia. Patients develop sudden, painless loss of vision and a pale fundus with a bright red spot over the fovea. In appropriate candidates, intra-arterial thrombolytic therapy is considered if symptoms are only of a few hours duration. Conservative measures include vigorous massage of the eye, administration of a vasodilator, and aspiration of aqueous humor. Amaurosis fugax can occur in patients with marked thrombocytosis (platelet count >800,000/mL) caused by myeloproliferative diseases, especially essential thrombocythemia or polycythemia vera. Management of cerebral metastasis: Evidence-based approach for surgery, stereotactic radiosurgery and radiotherapy. The bones most frequently involved with metastases are the femur, pelvis, spine, and ribs. Tumor cells may metastasize to vertebral bodies or the skull without entering the systemic circulation by seeding through Batson vertebral venous plexus (a valveless system of veins along the entire vertebral column that communicates with other venous systems, from the pelvis to the brain). The relative balance of osteoclastic and osteoblastic activity determines whether a lesion is osteolytic or osteoblastic. Malignant cells secrete many factors known to both stimulate the proliferation and activity of osteoclasts and produce osteolysis, possibly indirectly through the osteoblasts. A relatively small number of different malignancies account for most tumors that spread to bone. Carcinomas of unknown primary site, lung, breast, kidney, prostate, and thyroid; plasmacytoma; melanoma; and occasionally Ewing sarcoma b. Certain carcinomas have a predilection for metastasizing to particular skeletal sites. For example, skeletal metastases to the hands are unusual, but about 50% of these metastases arise from a lung primary. Types of bone metastases and their occurrence in various tumors are shown in Table 33. Osteolytic lesions are characterized by specific radiolucent areas: myeloma and commonly in renal cell and breast carcinomas. Osteoblastic lesions are characterized by radiopaque areas: commonly in prostate cancer. Bone metastases are usually confined within the bony substance and generally do not cross joint spaces. They lead to pain, pathologic fracture, neurologic compromise, and progressive immobility. Crippling bone disease can make bedridden patients susceptible to decubitus ulcers, hypercalcemia, and infections. Cervical spine metastases compressing the cord may result in myelopathy and weakness of the muscles of respiration, resulting in paralysis, pneumonia, and possibly death. Pathologic fracture is less likely in the osteoblastic variant of metastatic prostate cancer. The median survival of patients with breast cancer and only skeletal metastases, however, is 2 years. About 20% of patients with skeletal metastases from prostate cancer survive 5 years. Dull, aching, or boring pain that is worse at night than with physical activity is characteristic of pain from bone metastases. This pain pattern also occurs with malignant invasion of retroperitoneal structures without bony involvement. These characteristics are directly opposite to the typical pain of degenerative diseases, in which pain related to activity is present earlier and worse than pain at rest. Bone pain intensified by activity is often the first symptom of imminent fracture. Patients often report falling down, but it is often not clear whether the fracture was the cause or the effect of the fall. Spinal instability secondary to bone loss can cause excruciating pain, which is mechanical in origin. C-7 to T-1 vertebral pain is usually referred to the interscapular region; radiography of both cervical and thoracic spines is essential in these patients. T-12 to L-1 vertebral pain is usually referred to the iliac crest or sacroiliac joint. The pain typically is exacerbated by sitting or lying down and relieved by standing. Serum alkaline phosphatase levels are usually elevated in patients with bone metastases. Elevations appear to reflect an osteoblastic (or healing) response to tumor destruction. In pure osteolytic tumors, such as plasma cell myeloma, the serum alkaline phosphatase level is normal. Nonneoplastic causes of increased bone alkaline phosphatase include primary hyperparathyroidism, thyrotoxicosis, acromegaly, renal disease, Paget disease, osteomalacia, and healing fractures. Physiologic increases occur in the pediatric age group (before bony epiphyseal closure) and pregnancy (placental source). Radionuclide bone scan, using 99mTc-methylene bisphosphonate, is the most effective screening test for skeletal metastases. The scan often detects metastases several months before radiologic changes are evident. Radionuclide bone scans reflect osteoblastic activity; thus, purely osteolytic lesions with a preponderance of osteoclastic activity, such as in patients with myeloma, may not be apparent on a bone scan. Patients with a known cancer and bone pain have positive bone scans in 60% to 70% of cases; patients without bone pain have positive scans in 10% to 15% of cases. Plain radiographs remain essential for the diagnosis and characterization of bone metastases. Metastatic lesions must involve 30% to 50% of bone matrix to be visualized on plain radiographs. Diffuse osteoporosis may be the only radiologic abnormality in some patients with extensive bony involvement. Skeletal infections with pyogenic bacteria are frequently associated with sclerotic reactions; chronic granulomatous infections, however, may result in purely osteolytic lesions. Radiographs should be obtained and compared with previous films of the involved areas in patients with bone pain, abnormalities on physical examination suggestive of fracture, or asymptomatic abnormalities in bone scans. Routine complete skeletal surveys are not indicated except in patients with plasma cell myeloma, which may be associated with painless osteolytic lesions in crucial bone sites, such as the femora or cervical spine. Vertebral involvement from metastatic cancer is manifested by loss of the pedicles or lateral spinous processes and vertebral collapse with sparing of the intervertebral space. Postirradiation osteitis produces irregular, diffuse (rather than localized) osteolytic or mixed lesions confined to the radiation portal. In addition, they are useful to evaluate epidural compression, the extent of metastases. This technique is also ideal for demonstrating the intraosseous extension of tumor in to the cancellous bone. If a fracture has already occurred, care must be taken to sample the tumorous area adequately rather than the healing area of fibrous tissue and osteoid formation. If only a single bone is involved, the biopsy must be approached as if the lesion were resectable for cure. If other sites associated with a lower risk for morbidity are not available, bone biopsy for the differential diagnosis of cancer is indicated in patients with the following conditions: (1) An isolated bone lesion that the radiologist interprets as being compatible with a primary bone tumor (2) An osteolytic bone lesion in a crucial area. Bone biopsy should not be done in asymptomatic patients known to have cancer but with isolated, osteolytic lesions in noncrucial areas that are suspected to be benign lesions or metastatic disease. If a cancer is discovered, it is a metastasis for which treatment could have awaited the development of symptomatic disease. Medical management is necessary in patients with multiple painful metastatic sites. Chemotherapy and endocrine therapy are useful for treating metastatic tumors known to respond to these modalities. Chemotherapy doses may need to be attenuated because of compromised marrow function from neoplastic invasion or irradiation. Pyrophosphonates are natural compounds that are potent inhibitors of osteoclast-mediated bone resorption and contain two phosphonate groups bound to a common oxygen. Bisphosphonates (such as pamidronate or clodronate) are analogs of the endogenous pyrophosphonate with a carbon replacing the oxygen atom. The wide variety of alternative carbon substitutions results in marked differences in antiresorptive properties and side effects.

Branches from the mandibular division also innervate the tensor tympani and tensor palati as well as the anterior belly of the digastric and the mylohyoid muscles gastritis diet ����� purchase 20 mg bentyl otc. Within the nucleus of the spinal tract the fibres from the most anterior part of the face synapse in the caudal part of the nucleus gastritis diet ����� best buy bentyl, those from the posterior part most cranially gastritis symptoms bad breath discount 20mg bentyl with mastercard, and the rest in the region of the nucleus in between chronic gastritis juice order bentyl 20 mg online. The central fibres from the nuclei decussate and ascend as the trigeminal lemniscus to the thalamus from where the impulses are relayed to the postcentral gyrus gastritis diet ���������� purchase bentyl 20 mg amex. Sensory and motor roots of the trigeminal nerve the two roots emerge from the pons gastritis diet ��������� buy generic bentyl, pass though the pontine cistern and enter the middle cranial fossa where the sensory root has the trigeminal ganglion. Trigeminal ganglion Most of the cell bodies of the sensory root are located in the trigeminal ganglion, which is also called the semilunar ganglion or the Gasserian ganglion. The ganglion lies near the apex of the petrous temporal bone inside the trigeminal cave, a pocket of dura invaginated from the posterior cranial fossa. Medially the ganglion is related to the internal carotid artery and the cavernous sinus. It can be blocked by introducing a needle through the foramen ovale, which is close to the ganglion. The motor root of the trigeminal nerve and the greater petrosal nerve lie deep to the ganglion. From the convex surface of the ganglion, which is pointing laterally, emerge the three peripheral divisions of the trigeminal nerve: the ophthalmic, the maxillary and the mandibular nerves. The nucleus of the abducent nerve lies in the floor of the fourth ventricle in the upper part of the pons. The fibres of the facial nerve wind round the nucleus to form the facial colliculus. The abducent nerve emerges on the brainstem at the junction between the medulla and pons. It then passes forward through the pontine cistern, pierces the dura mater to enter the cavernous sinus, where it lies on the lateral aspect of the internal carotid artery. The nerve enters the orbit through the tendinous ring at the superior orbital fissure and supplies the lateral rectus muscle. The intracranial course of the abducent nerve is long and so it is vulnerable at many sites. Ophthalmic nerve this nerve enters the cavernous sinus, lies on the lateral wall and passes to the orbit through the superior orbital fissure. Its branches supply the conjunctiva, cornea, the upper eyelid, the forehead, the nose and the scalp. It also conveys parasympathetic fibres to the lacrimal gland, glands in the nasal cavity, submandibular and sublingual glands, and transmits taste fibres from the anterior two-thirds of the tongue. From the nucleus, motor fibres loop around the abducent nerve nucleus (facial colliculus) and emerge at the cerebellopontine angle along with the nervus Maxillary nerve From the middle cranial fossa, the maxillary nerve enters the pterygopalatine fossa through the foramen rotundum. The sensory fibres in the nervus intermedius are the central processes of the geniculate ganglion, and these fibres synapse in the nucleus of the tractus solitarius in the pons. The nervus intermedius lies lateral to the motor fibres of the facial nerve, in between the latter and the vestibulocochlear nerve. The motor fibres of the facial nerve and the nervus intermedius pass through the pontine cistern and enter the internal acoustic meatus where the two join together to form the facial nerve. Here the nerve runs laterally over the vestibule to reach the medial wall of the middle ear, where it bends sharply backwards over the promontory. It passes downwards on the posterior wall of the middle ear to emerge though the stylomastoid foramen at the base of the skull. The chorda tympani nerve carries parasympathetic fibres to the submandibular and sublingual glands as well as taste fibres from the anterior two-thirds of the tongue. Before entering the parotid gland the nerve supplies branches to the posterior belly of the digastric, stylohyoid and the muscles of the auricle. Infranuclear paralysis of the facial nerve has a wide variety of causes such as acoustic neuroma and its surgery, viral infection producing inflammation and swelling of the nerve, fractures of the base of the skull, and tumours and surgery of the parotid gland. Supranuclear paralysis, which affects the contralateral facial muscles, spares the orbicularis oculi and the muscles of the scalp, since the part of the facial nerve nucleus supplying these has bilateral cortical connections. The glossopharyngeal nerve emerges on the brainstem in the groove between the olive and the inferior cerebellar peduncle. In the jugular foramen the nerve has two ganglia which contain the cells of origin of its sensory fibres. On emerging from the foramen it gives off the tympanic branch which, after supplying the middle ear, continues as the lesser superficial petrosal nerve carrying parasympathetic fibres to the otic ganglion to supply the parotid gland. In the upper part of the neck the nerve accompanies the stylopharyngeus muscle and enters the pharynx by passing between the middle and superior constrictor muscles. Its terminal branches supply the posterior third of the tongue and the tonsillar fossa (oropharynx). The nerve also supplies the stylopharyngeus muscle; its parasympathetic fibres innervate the parotid gland. In the medulla the glossopharyngeal nerve has the following nuclei: fibres from the mucosa of the pharynx and larynx and those transmitting visceral sensation of the organs in the thorax and abdomen; fibres carrying general sensation from the dura, parts of the external auditory meatus, external surface of the tympanic membrane; and taste fibres from the epiglottis. The cranial part of the accessory nerve which innervates the muscles of the soft palate, pharynx and larynx also is distributed via the vagus. This is situated in the floor of the fourth ventricle in the medulla and receives the general visceral sensation from the various organs supplied by the vagus. Beyond the inferior ganglion the cranial part of the accessory nerve joins the vagus. The former arises from the nucleus ambiguus and emerges along with the fibres of the vagus from the brainstem. It then joins the spinal root for a short distance and branches off to rejoin the vagus to be distributed to the muscles of the soft palate, pharynx and larynx. The spinal root arises from the upper five segments of the cervical part of the spinal cord and enters the skull through the foramen magnum, where it joins the cranial root, and leaves the skull through the jugular foramen. Immediately below the jugular foramen the spinal root passes backwards to supply the sternocleidomastoid and trapezius. Its nucleus, which gives rise to the somatic motor fibres, lies in the medulla in the floor of the fourth ventricle. The nerve emerges as rootlets in the groove between the pyramid and the olive; the rootlets unite to form the nerve, which leaves the skull through the hypoglossal canal. In the neck the nerve first lies between the internal jugular vein and the internal carotid artery, crosses superficial to the latter and the external carotid, and passes forward deep to the mylohyoid muscle to supply the muscles of the tongue. Division of the hypoglossal nerve or lesions involving its nucleus will result in an ipsilateral paralysis and wasting of the muscles of the tongue. Clinically, this is detected by deviation of the protruded tongue to the affected side. Supranuclear paralysis due to an upper motor neurone involving the corticobulbar pathways will lead to paralysis but not atrophy of the muscles on the contralateral side. The lower part of the cord is tapered to form the conus medullaris from which a prolongation of pia mater, the filum terminale, extends downwards to be attached to the coccyx. In the third month of intrauterine life the spinal cord fills the whole length of the vertebral canal, but from then on the vertebral column grows more rapidly than the cord. At birth the cord extends as far as the third lumbar vertebra and reaches its adult level gradually. The dura mater, which is continuous with that of the brain, extends up to the second sacral vertebra. The arachnoid mater lines the inner surface of the dura, and the pia mater is adherent to the surface of the cord. The epidural space outside the dura contains fat and the components of the vertebral venous plexus. The spinal cord is suspended in the dural sheath by the denticulate ligaments (ligamentum denticulatum. These, having a serrated lateral edge, form a shelf between the dorsal and ventral roots of the spinal nerves. The cord has on its surface a deep anterior median fissure and a shallower posterior median sulcus. It also has, on either side, a posterolateral sulcus along which the dorsal roots of the spinal nerves are attached. The area of the spinal cord from which a pair of spinal nerves are given off is defined as a spinal cord segment. The cord has 31 pairs of spinal nerves and hence 31 segments: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral and 1 coccygeal. The dorsal (posterior) root of the spinal nerve which carries sensory fibres has a dorsal root ganglion which has the cells of origin of the dorsal root fibres. The ventral (anterior) root, which is motor, emerges on the anterolateral aspect of the cord on either side. The anterior and posterior roots join together at the intervertebral foramen to form the spinal nerve which, on emerging from the foramen, divides immediately in to the anterior and posterior rami, each containing both motor and sensory fibres. The lumbar and sacral nerve roots below the termination of the cord form the cauda equina. Internal structure of the spinal cord the grey matter containing the sensory and motor nerve cells is surrounded by the white matter with the ascending and descending tracts. In a transverse section the grey matter is seen as an H-shaped area containing in its middle the central canal. The posterior (dorsal) horn of the grey matter has the termination of the sensory fibres of the dorsal root. The larger anterior (ventral) horn contains motor cells which give rise to fibres of the ventral roots. In the thoracic and upper lumbar regions there are lateral horns which have the cells of origin of the preganglionic sympathetic fibres. A few of the major tracts are briefly described below: synapses in the cuneate nucleus, from where secondorder neurons proceed to the higher centres after crossing in the sensory decussation. Lateral corticospinal tract (crossed pyramidal tract) A major tract in the lateral funiculus is the lateral corticospinal tract. The corticospinal tracts control skilled voluntary movements and consist of axons of neurons in the frontal and parietal lobes. These descend through the internal capsule, the basis pedunculi of the midbrain, the pons, the pyramid of the medulla and then decussate in the motor decussation in the lower part of the medulla oblongata. The majority of fibres cross to the opposite side and descend as the lateral corticospinal tract. The lateral corticospinal tract thus contains axons of neurons of the contralateral cerebral hemisphere. These fibres terminate at different levels, forming synaptic connections with motor neurons. The fibres in the tract are somatotopically arranged, fibres for the lower part of the cord laterally and those for the upper levels medially. Fasciculus gracilis (of Goll) and fasciculus cuneatus (of Burdach) these two tracts form the major components of the dorsal column. They contain fibres subserving fine and discriminative tactile sensation as well as proprioception. As the spinal cord is ascended the fibres are added to the lateral part of the dorsal column. Hence the fasciculus gracilis deals mostly with sensation from the lower limb and the fasciculus cuneatus with the upper limb. Fibres in the dorsal columns are uncrossed, carrying sensation from the same side of the body. Axons cross in the midline in the ventral grey commissure close to the central canal. Many of the fibres as they ascend give collaterals to the reticular nuclei in the brainstem and finally terminate in the thalamic nuclei. The fibres are somatotopically arranged, those for the lower limb superficial and those concerned with the upper limb deepest. Fibres carrying pain and other sensations from the internal organs are carried in the spinoreticular tract, which terminates in the reticular formation in the medulla and pons. The ventral root of the spinal nerve contains motor fibres whose cell bodies are in the ventral horn of the spinal cord. The sensory fibres in the dorsal root have their cells of origin in the dorsal root ganglion. They join together to form the spinal nerve in the intervertebral foramen, and immediately beyond the foramen the spinal nerve divides in to the dorsal ramus and the ventral ramus. With the exception of the first two cervical spinal nerves the ventral rami are larger than the dorsal rami. All dorsal rami pass backwards to innervate the muscles of the back, the ligaments and the joints of the vertebral column. They also supply cutaneous branches to the skin of the posterior aspect of the head, trunk and gluteal region. Each intercostal nerve innervates the muscles of its intercostal space and the overlying skin. The lower six intercostal nerves extend out to the anterior abdominal wall to innervate the muscles and the overlying skin in a segmental fashion.

Sumatriptan also should not be used within 24 hours of administration of an ergotaminecontaining medication gastritis diet ������� order genuine bentyl on-line. Patients with aneurysms or arteriovenous malformations can present clinically as migraine patients gastritis diet ���� order bentyl in united states online. If there is something different about the severity or nature of this headache gastritis symptoms treatment mayo clinic best purchase for bentyl, consider the possibility of a subarachnoid hemorrhage diet gastritis adalah order bentyl cheap. Headaches that are always on the same side and in the same location are very suspicious for an underlying structural lesion gastritis healing process purchase line bentyl. To help reassure patients gastritis stool buy cheap bentyl 20mg, it can be noted that isolated headache was the first and only clinical symptom in just 8. Many patients seeking narcotics have learned that faking a migraine headache is even easier than faking a ureteral stone, but they usually do not follow the typical course of falling asleep after being given a shot and waking up a few hours later with pain relief. Paper presented at the 55th Annual meeting of the American Academy of Neurology, Honolulu, Hawaii, April 8, 2003. The patient may complain of an "aura," feel he is "about to have a seizure," experience a brief petit mal "absence," exhibit the repetitive stereotypical behavior of complex partial seizures, display the whole-body tonic stiffness or clonic jerking of generalized (grand mal) seizures, or simply be found in the gradual recovery of the postictal confusion and lethargy. Patients experiencing generalized tonic-clonic seizures can injure themselves, most often by biting the tongue laterally or by having an unprotected fall. Usually, only suctioning or turning the patient on his side is required, but breathing will be uncoordinated until the tonic-clonic phase is over. With a prolonged seizure, this treatment should be followed by loading with phenytoin (Dilantin) or fosphenytoin (Cerebyx) to prevent recurrence of seizures. If the patient arrives in the postictal phase, examine thoroughly for injuries and signs of systemic disease that can provoke seizures. Record a complete neurologic examination, the results of which are apt to be bizarre. Repeat the neurologic examination periodically, looking for findings suggestive of focal brain disease. If the patient is indeed recovering, you may be able to obviate much of the diagnostic workup by waiting until he is lucid enough to give a history. Postictal inability to arouse may last 10 minutes after a generalized tonic-clonic seizure, with confusion typically lasting less than 30 minutes. If the patient arrives awake and oriented after a presumed seizure, corroborate the history through witness accounts or the presence of injuries, such as a scalp laceration, a bitten tongue, or the presence of urinary or fecal incontinence. Doubt a generalized tonic-clonic seizure if there is no typical postictal recovery period. Investigate for alcohol or substance abuse; withdrawal from alcohol, benzodiazepines, or barbiturates can provoke seizures. If the patient has a history of seizure disorder or is taking anticonvulsant medications, check his records and determine current and past frequency of seizures. Speak to his physician, and find out whether a cause has been determined and what studies have been performed. Reasons for decreasing alcohol consumption may include inability to afford alcohol, suffering from pancreatitis or gastritis causing inability to consume alcohol (requiring further evaluation and treatment), or, the patient may have decided to try to stop drinking, realizing it is bad for him. If the patient is requesting detoxification, he should be supported in this decision both medically and emotionally, and additional recovery resources should be discussed. If a patient is demonstrating signs of delirium tremens, such as tremors, tachycardia, and hallucinations, withdrawal should be medically supervised and treated with benzodiazepines. However, thiamine has been shown to be beneficial in preventing coma and death as a result of Wernicke encephalopathy in patients presenting with altered mental status. Administration of thiamine and vitamins is inexpensive, and has very few side effects. Given this, it is advisable to treat alcoholic patients presenting with acute delirium for both alcohol withdrawal and thiamine deficiency. If the seizure is a new event, obtain a serum glucose level ( to confirm a rapid bedside test result) as well as serum electrolyte concentrations (sodium, calcium, magnesium), renal function tests, hepatic function tests (if liver impairment is suspected), complete blood cell count (if infection is suspected), and urine toxicology screen (if drugs of abuse are suspected). Lumbar puncture should be performed when fever, persistent altered mental status, or nuchal rigidity indicates a possibility of meningitis or encephalitis. If the patient has an established seizure disorder, blood tests are not routinely needed when the patient has a single breakthrough seizure. Anticonvulsant drug levels should be checked when toxicity or noncompliance is suspected. Finding a level below the reported therapeutic range should not prompt a dose increase in a patient who has been seizure free for a prolonged period. A neurologist should be consulted before antiepileptic drug treatment is initiated for brief new-onset seizures. The neurologist may want to make a detailed evaluation of the patient and counsel him regarding risk for seizure recurrence, the advantages and disadvantages of anticonvulsant therapy, and the psychosocial effect of another seizure. Patients with a single, brief, uncomplicated seizure, a normal neurologic examination, no comorbidity, and no known structural brain disease need not be started on any antiepileptic drug prior to outpatient referral. They should take showers rather than baths, not swim without supervision, and not work at heights. Driving should also be restricted until an appropriate seizure-free period has elapsed, specified 6 to 12 months in most states. If the neurologist recommends phenytoin loading in a stable awake patient, an acceptable oral regimen can be prescribed. Give 1 g of phenytoin capsules divided in to three doses (400 mg, 300 mg, 300 mg) administered at 2-hour intervals. The ubiquitous padded throat sticks may be nice for a patient to hold and to bite on at the first sign of a seizure, but they do nothing to protect the airway and are ineffective when the jaw is clenched. It is diagnostically useful to see how the seizure resolves without medication aid; also, the patient will awaken sooner if he has not been medicated. Do not wait 30 minutes before initiating anticonvulsant therapy for a patient having a continuous seizure or not awakening between intermittent seizures (old definition of status epilepticus). For practical purposes, a seizure lasting longer than 5 minutes should be treated as generalized convulsive status epilepticus, because a generalized tonic-clonic seizure lasting longer than 5 minutes is unlikely to stop spontaneously. Ethanol abusers sustain more head trauma and seizure disorders than does the population at large. Both are ineffective (and unnecessary because the problem is self limiting) and can themselves produce withdrawal seizures. Do not rule out alcohol withdrawal seizures on the basis of a high serum ethanol level. Even patients with genuine epilepsy occasionally fake seizures for various reasons, and an exceptional performer can be convincing. Amateurs may be roused with ammonia or smelling salts, and few can simulate the fluctuating neurologic abnormalities of the postictal state. Probably no one can voluntarily produce the pronounced metabolic acidosis or serum lactate elevation of a grand mal seizure (see Chapter 4). Except for rare instances, seizures are not predictable and can occur at inconvenient, embarrassing, or even dangerous times. Seizures are usually short, lasting less than 5 minutes, but can be preceded by a prodromal phase and followed by a long postictal phase, during which there is a gradual return to baseline. Seizures have been referred to as either grand mal seizures (convulsive movements) or petit mal seizures (staring without convulsive movements). Epilepsy is a disease characterized by spontaneous recurrence of unprovoked seizures. Provoked seizures result from transient alterations in brain metabolism in an otherwise normal brain. Some factors that can trigger such seizures are hypoglycemia, hyponatremia, hypocalcemia, alcohol and illicit drug withdrawal, meningitis, encephalitis, stroke, and certain toxins and toxic drugs. The new terminology for seizures divides them in to two classes: generalized seizures and partial seizures. With generalized seizures, there is a complete loss of consciousness at onset of the seizure. Partial seizures are characterized by retention of consciousness, because they begin in a limited brain region. There are seven types of generalized seizures, which start throughout the entire cortex at the same time and, therefore, cause loss of consciousness. They are the following: n n Atonic seizures, characterized by sudden loss of muscle tone and subsequent falling or dropping to the floor unprotected (drop attacks). In simple partial seizures, only one neurologic modality is affected during the seizure. The resulting symptoms depend on the area of the brain cortex from which the seizure arises. Complex partial seizures (psychomotor or temporal lobe seizures) are associated with alteration, but not loss, of consciousness. The patient is awake and staring blankly but is not responsive to external stimuli. These seizures may be accompanied by automatism (repetitive, purposeless movements, such as lip smacking and chewing, hand wringing, patting, and rubbing) and last 30 to 50 seconds. Generalized tonic-clonic seizures are frightening and inspire observers to "do something," but usually it is necessary only to stand by and prevent the patient from injury. The age of the patient is associated with the probable underlying cause of a first seizure and therefore is a factor in disposition. In the 12- to 20-year-old patient, the seizure is probably "idiopathic," although other causes are certainly possible. In the 40-year-old patient experiencing a first seizure, neoplasm, posttraumatic epilepsy, and withdrawal must be excluded. In the 65-year-old patient experiencing a first seizure, cerebrovascular insufficiency must also be considered. With elderly patients, the possibility of an impending stroke, in addition to the other possible causes, should be kept in mind during treatment and workup. Absence (petit mal) seizures, which are manifested as brief (1 to 10 seconds) episodes of staring and unresponsiveness. These seizures, unlike complex partial seizures, are rarely found in adults, are very brief, do not produce postictal confusion, and occur very frequently (up to 100 per day). Atypical absence seizures, which are similar to absence seizures but last longer and often include more motor involvement. A toxic screen may be needed to detect the many drug overdoses that can present as seizures, including overdoses of drugs such as amphetamines, cocaine, isoniazid, lidocaine, lithium, phencyclidine, phenytoin, and tricyclic antidepressants. The parents may have been horrified by the sight of their child becoming cyanotic with breathing difficulty, unresponsiveness, and jerking eye movements during the seizure. The child may be found to have a fever, and there may be a family history of febrile seizures. A vaccination with diphtheria and tetanus toxoids and whole-cell pertussis vaccine may have been administered earlier in the day or 1 to 2 weeks following a measles, mumps, and rubella vaccination. Inquire in to recent condition(s) and medical history, as well as any family history of seizure disorders. Have witnesses describe the event in detail, including the type of motor and eye movements, changes in breathing and skin color, and whether or not there was complete loss of consciousness or incontinence. Perform a physical examination that includes evaluation of pupil size and reactivity, along with funduscopy to look for retinal hemorrhage, which would suggest intentional injury. After the patient has experienced full recovery from the postictal state, the physical examination should be entirely normal. In children older than 6 months of age, in the absence of a history of illness, vomiting or diarrhea, or suspected ingestion, routine laboratory testing is not needed. Infants younger than 6 months of age require immediate glucose testing to rule out hypoglycemia. Serum sodium, calcium, and magnesium levels should also be determined to rule out low levels of these electrolytes. Toxicology screening should be considered if there is suspicion of toxin exposure. Children who have just one unprovoked seizure-for whom there is no suspicion of trauma, infection, or intoxication-and who have returned to their baseline state, may be discharged with appropriate medical follow-up. Parents should be appropriately reassured and informed that 60% of such children never have a recurrence. If seizure activity persists for more than 5 minutes, consider bag-valve-mask ventilation or intubation if there is significant respiratory compromise. In the febrile child: A careful history and physical examination should be done to identify a possible source of the fever and to rule out any evidence of trauma. Children with fever without an identifiable source should be evaluated for urinary tract infection. In patients whose level of consciousness has not returned to baseline; who have a bulging fontanel, a positive Kernig or Brodzinski sign, photophobia, severe headache, or pretreatment with antibiotics; or who are lethargic or irritable, lumbar puncture should be performed to exclude meningitis. Children who are younger than 6 months of age must be evaluated for metabolic abnormalities, underlying neurologic disorders, meningitis, and encephalitis. Antipyretics have not been found to be effective in preventing the recurrence of febrile seizures. Benzodiazepines are also probably of no practical benefit when used for prophylaxis. There is no evidence that children with simple febrile seizures have any difference in cognitive outcomes than children without such seizures, and although these seizures appear frightening, they are generally harmless. Parents should be reassured and given written, detailed information about febrile seizures and then referred back to their primary care physician for follow-up.

If the patient returns with mild oozing of blood from around an anterior pack gastritis diet questionnaire discount bentyl generic, you may be able to stop the bleeding without removing the pack gastritis from stress discount bentyl online american express. Try injecting a vasoconstrictor directly in to the sponge (not in to the patient) gastritis snacks discount 20mg bentyl, or adding air to a nasal balloon pack gastritis diet ��� proven 20 mg bentyl. When removing a compressed cellulose sponge pack chronic gastritis forum buy bentyl 20mg free shipping, soften it with 1 to 2 mL of water or saline and wait 5 minutes gastritis diet ������ discount bentyl 20mg without a prescription, thereby reducing trauma, pain, and the incidence of rebleeding. What Not To Do: Because of the nasopulmonary reflex, arterial oxygen pressure will drop about 15 mm Hg after the nose is packed. With packing in place, these patients are at risk for desaturation and may need admission. Do not waste time trying to locate a bleeding site if brisk bleeding is obscuring your vision in spite of vigorous suctioning. Have the patient blow out any clots and insert the medicated cotton pledgets immediately or go directly to anterior packing. Do not order routine clotting studies unless there is persistent or recurrent bleeding, use of anticoagulants or other evidence of an underlying bleeding disorder. Do not cauterize or place a painful device in the nose before providing adequate topical anesthesia unless rapid hemorrhaging requires it. It will only serve as a plug in the anterior nares rather than as a hemostatic pack. Do not discharge a patient as soon as the bleeding stops, but keep him for 15 to 30 minutes more. Posterior epistaxis typically stops and starts cyclically and may not be recognized until all of the aforementioned treatments have failed. Children tend to bleed secondary to nose picking; adolescents bleed secondary to facial trauma associated with athletic activity or fighting. Epistaxis in the middle-age patient is more often the harbinger of neoplastic disease. Nosebleeds in the elderly are generally the result of underlying vascular fragility in combination with blood-thinning medications. Nosebleeds are more common in winter, no doubt reflecting the low, ambient humidity indoors and outdoors and the increased incidence of upper respiratory tract infections. In contrast, posterior bleeding may be asymptomatic or may present insidiously as nausea, hematemesis, anemia, hemoptysis, or melena. Causes of epistaxis are numerous; dry nasal mucosa, nose picking, and vascular fragility are the most common causes, but others include trauma, foreign bodies, blood dyscrasias, nasal or sinus neoplasm or infection, septal deformity or perforation, atrophic rhinitis, hereditary hemorrhagic telangiectasis, and angiofibroma. Epistaxis that results from minor blunt trauma in healthy individuals rarely requires any intervention and will spontaneously subside with head elevation alone and avoidance of any nasal manipulation. Specific antihypertensive therapy is rarely required and should be avoided in the setting of significant hemorrhage. Hereditary hemorrhagic telangiectasia is the most common systemic disorder of the vascular system that affects the nasal mucosa. Blood dyscrasias can be found in patients with lymphoproliferative disorders, immunodeficiency, systemic disease, or in the alcoholic patient. Thrombocytopenia can lead to spontaneous mucous membrane bleeding, with platelet counts of 10,000/mm3 to 20,000/mm3. One study of chronic nosebleeds in children showed that a third of these patients can be expected to have a coagulation disorder. Because of the nasopulmonary reflex, arterial oxygen pressure will drop about 15 mm Hg after the nose is packed, which can be troublesome in a patient with heart or lung disease and often requires hospitalization and supplemental oxygen. At times, the history is not revealed, and the child simply presents with a purulent discharge, pain, bleeding, or hearing loss. An adult might have a pencil eraser or "Q-tip" come off in the ear canal while trying to remove earwax. Most dramatically, a panic-stricken patient arrives complaining of a "bug crawling around" in his ear. There may be severe pain if the object or insect has scratched or stung the canal or tympanic membrane. What To Do: Use an otoscope to inspect the ear canal while pulling up and back on the pinna to help straighten the ear canal, thereby providing a better view. Mineral oil, 2% lidocaine (Xylocaine), or benzocaine/antipyrine (Auralgan) works well. If a hard or spherical object remains tightly wedged in the canal, attempt to roll the foreign body out by getting behind it with a right-angle nerve hook, ear curette, or wire loop. An alternative removal technique is to take a drop or two of cyanoacrylate (Super Glue, Dermabond), and place it on the end of the wooden shaft of a cotton swab. A small magnet or iron-containing metallic foreign body can be removed by touching a pacemaker magnet to a metal forceps and then, at the same time, touching the forceps to the foreign body, withdrawing all of the magnetized objects together. Alligator forceps are good for grasping soft objects, such as cotton, paper, and certain insects. There should be no delay in removing a foreign body in a canal when there is an obvious infection or when the foreign body is a disk or button battery. Do not irrigate or instill liquids in to the ear canal, because on contact with moist tissue, the alkaline battery is capable of producing a liquefactive necrosis extending in to deep tissues within hours. At any time, if a child becomes uncooperative, especially when using metal instruments, use procedural sedation as described in Appendix E. Ketamine sedation appears to have a positive effect on the success rate of foreign body removal in children. Do not attempt to irrigate a canal filled with a bean or other object that may swell with hydration. The bony canal will slowly close the forceps as they are advanced, and the object will be pushed farther in to the canal. Alligator forceps are designed for use in the canal, but even they will push a large, hard foreign body farther in to the ear. The cross-section of the canal is elliptic; therefore the physician can usually find an opening around a circular foreign object in which to place an instrument or for water to get behind when irrigating. Some physicians do not recommend the use of a Waterpik for irrigation, because the high-pressure water jet has the potential for rupturing the tympanic membrane. When the foreign body within the ear canal is a cyanoacrylate adhesive (Super Glue, Dermabond), it can be removed more easily after 48 hours when desquamation occurs. On telephone consultation, patients can be instructed to use cooking or baby oil, or ethyl or isopropyl alcohol, instilled in to the ear canal, to kill an insect at home. Complications of foreign body removal from the ear canal include trauma to the skin of the canal, canal hematoma, otitis externa, tympanic membrane perforation, or ossicular dislocations and, rarely, facial nerve palsy. Sometimes, however, the history is obscure, and the child presents with local pain; a purulent, unilateral nasal discharge; epistaxis; a nasal voice change; or foul breath. The most commonly encountered nasal foreign bodies are beans, peanuts or other foodstuffs, beads, toy parts, pebbles, paper wads, and eraser tips. These objects usually lodge on the floor of the nose just below the inferior turbinate or immediately anterior to the middle turbinate. These include suction, air pressure, ear curettes, curved hooks, alligator forceps, bayonet forceps, balloon catheters, irrigation and glue. Before attempting removal techniques in an uncooperative patient, consider use of sedation. Because of the potential for spraying of body fluids from the nose, always practice universal precautions and wear appropriate eye and splash protection. Before any of the removal procedures, explain in detail what you are about to do to the patient and or parent. After initial inspection with a nasal speculum and bright light, suction out any discharge, and insert a small cotton pledget soaked in 4% cocaine or alternatively a 1:1 mixture of phenylephrine (Neo-Synephrine) and tetracaine (Pontocaine), which will shrink the nasal mucosa and provide topical anesthesia. If you cannot safely insert a pledget, drip or spray the same solution in to the nose. Further suctioning success may be obtained by placing a piece of soft plastic tubing over the end of the suction tip. Placing water-soluble lubrication on the end of this tubing will also help achieve a better vacuum seal. If an object cannot be grasped, it may be rolled out of the nose by using an ear curette or right-angle ear hook to get behind it. A soft-tipped hook can be made by bending the tip of a metal Calgiswab to a 90-degree angle. Button batteries can cause serious local damage through liquefaction necrosis and should be removed quickly. Button batteries of all sizes have a distinctive double contour on radiographs; therefore, with a high index of suspicion, radiographs can help assist with an uncertain diagnosis. Earring magnets that become stuck together across the nasal septum must also be removed as soon as possible because of the risk for pressure necrosis leading to septal perforation. Using the balloon catheter technique bilaterally, both magnets should be removed simultaneously to prevent a lone magnet from dropping back in to the nasopharynx and being aspirated. Small, particulate material may be irrigated from the nasal cavity by insertion of an irrigation syringe in to one nostril while the patient sits up, leans forward, and repeats "eng" as you irrigate. What Not To Do: Do not inspect the nasal cavity by opening the nasal speculum in the horizontal plane. The speculum should be opened in the vertical plane and not pressed against the nasal septum. These objects can cause quick tissue necrosis and must be removed as soon as possible. If you suspect a button battery in the nose but cannot find it, consider a radiograph for confirmation. Most nasal foreign bodies can be removed easily and safely by emergency clinicians. There is time available to provide procedural sedation, if necessary, as well as to assemble all of the supplies and instruments necessary to help ensure the success of this procedure. The mucous membrane lining the nasal cavity allows the tactical advantages of vasoconstriction and topical anesthesia. If the object has been aspirated in to the tracheobronchial tree, it may produce coughing and wheezing, and bronchoscopy under anesthesia is required for retrieval. Animate foreign bodies (myiasis) of the nose are common in warm tropical climates and are associated with poor hygiene. These maggots can cause varying degrees of inflammatory reaction, including local tissue destruction, fetid discharge, and pain. Inspection after suctioning may reveal constant motion and masses of different worms. Those with dentures, especially full dentures, are more likely to swallow a bone because of reduced sensitivity and inability to chew properly. Fish bones, which are usually long, are commonly caught in the oropharynx, particularly at the region of the tonsils and the tonsillar pillars. At these regions, fish bones can usually be grasped and extracted, as long as they can be visualized. Obstruction of the esophagus produces drooling and causes the patient to spit up whatever fluid is swallowed. If complete or nearcomplete obstruction is present, immediate intervention with direct visualization using a laryngoscope and removal with an instrument, such as a McGill forceps, is indicated. Examine the anterior neck for tenderness, masses, or subcutaneous emphysema (suggests perforation). Place the tongue depressor at the middle third of the tongue and press firmly downward to give good exposure without making the patient gag. Objects at the base of the tongue or in the hypopharynx may require a mirror or indirect laryngoscope for visualization. They should be instructed to seek follow-up care as soon as possible if the pain worsens, fever develops, or if breathing or swallowing is difficult. An impacted button battery represents a true emergency and requires rapid removal, because leaking alkali produces liquefactive necrosis. A tablet composed of irritating medicine, if swallowed without adequate liquid, may stick to the mucosa of the pharynx or esophagus and cause an irritating ulcer with a foreign body sensation. If a foreign body is found in the pulmonary tree, a pulmonary specialist consultation should be obtained. Also inform him that if the symptoms worsen or fail to resolve in 2 days, he may need further endoscopic studies to look for a hidden problem. What Not To Do: Do not assume that a foreign body is absent just because the pain disappears after a local anesthetic is applied.

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