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Oncologic Emergencies

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Neutropenic Fever

always consider infection as the cause especially if ANC<500. Other sources say it it when the WBC count falls below 500 with a WBC<1000 as a grey zone. Still others assign ANC + Bands<500 as the breakpoint.   in other populations, neutropenia does not predispose to bacterial infections as much as the oncologic patient. This is because in addition to the decreased WBC, patients with cancer on chemotherapy often have decreased mucosal and physical barrier immunity.   Since there are very few WBCs, classic signs like infiltrates on c-xr or cells in the urine might not be present. A chest CT might be a better test than the C-XR as there have been numerous occasions of negative C-XR with positive CTs. Always obtain at least one set of cultures through a central line if one is present. Use a fourth generation cephalosporin or imipenem. Add vancomycin if:

  Neupogen should also be added, it has been proven to reduce duration and severity of episodes (Blood 1997;90(12):4710-8.) Admit to reverse isolation room. Some experts advocate adding AmphoB if the patient is still febrile at day 4 or 7 without a source

neutropenic enterocolitis

Typhlitis, also known as neutropenic enterocolitis or ileocecal syndrome,1 is an inflammatory process involving segments of terminal ileum, ascending colon, and cecum that could progress to ulceration, necrosis, and perforation. 2,3 This syndrome, clinically characterized by neutropenia, fever, and abdominal pain, seems to happen more frequently in patients with leukemia undergoing aggressively cytotoxic chemotherapy.4 Occasionally, neutropenic enterocolitis could also present in other immunocompromised patients, including malignant neoplasms,5 aplastic anemia,4 and acquired immunodeficiency syndrome6 in profound neutropenia state. In the review of the literature, only individual case reports7-9 of patients with acute leukemia with neutropenic enterocolitis before any chemotherapy had been demonstrated.

Mechanical Problems

Epidural Spinal Compression

Breast, Lung, Testicular, Kidney, and Prostate CA all met to bone. If a patient presents with back pain and a history of malignancy, assume spinal mets or cord compression until proven otherwise. Ask about worsening of symptoms at night, worsening with cough, or worse in the supine position.   Get a neurosurgery consult and give high dose steroids (decadron 1 mg/kg)

Superior Vena Cava Syndrome

Only an emergency if cerebral edema or laryngeal compression. Seen especially in small cell and lymphoma. Neck lines can also cause this entity by SVC thrombosis. Compression above the entry of the azygous may present with relatively few symptoms. Facial edema, Stokes sign (tight collar), plethora of face, edema of face. Pt will often complain of a sensation of fullness when leaning forward. Use legs for IVs. Should be visible on X-Ray. Pemberton’s Sign: raising the arm causes facial redness.   rx c radiation can be diagnosed by ultrasound thrombus usually causes critical closure use lytics under angio and then stent may need bypass  

Tumor Lysis Syndrome

1-5 days after radiation or chemo. Not assoc c solid tumors. Hyperuricemia, hyperphosphatemia (and 2nd hypocalcemia), hyperkalemia. HD if it gets really bad

Hyperviscosity syndrome

Normal viscosity is 1.4 to 1.8 x water. Symptoms begin when blood reaches 5 x that of water. Measured in centipoises (1 is viscosity of water) Caused by dysproteinemias such as Waldenstrom’s macroglobulinemia or Multiple Myeloma, Acute Leukemia with Blast Crisis, or P. Vera. Triad of bleeding, vision abnormality, Neurologic symptoms. Presentation can be mental status changes, unexplained dyspnea, or headache. If from multiple myeloma, can look for a globulin gap. Total protein-albumin >4. Leukopheresis or plasmapheresis and aggressive hydration. Phlebotomy of 2-3 units of blood can also be temporizing.

Neoplastic Cardiac Tamponade

Complication of lung, breast, lymphoma, or leukemia. Pericardial tamponade may be the initial presentation of malignancy (8 out of 23 cases of neoplastic tamponade had the event as the initial presentation (Chest 1985; 88(1)) Many patients will not present with the classic symptoms. 1/3 of patients will lack the classic findings (J Am Coll Cards 1991; 17(1)) Vague chest tightness, shortness of breath, and fatigue may be the only clues.

Acute Hyperleukocytosis Leukemia (AHL)

Tissue hypoperfusion secondary to elevated WBCs. Seen when total WBC approaches 100,000, but can be seen in monoblastic leukemia (AML) at levels from 25-50,000. Patients can present with shortness of breath, respiratory failure, and/or depressed mental status. t can also cause GI bleeding or hepatic failure.   Treat with aggressive IV hydration. Prepare for tumor lysis syndrome. Leukapheresis or whole blood phlebotomy can be used. Consult hematology for chemotherapy, such as Hydroxyurea. This agent will reduce the WBC count by 50% to 80% within 24 to 48 h. Its cytotoxic effect diminishes all cell lines Allopurinol must be started early for prophylaxis against hyperuricemia. Give 300 mg PO. Amphojel 30-60 cc PO (to proph against phosphate) Anticipate for and prepare hemodialysis. Alkalinization of urine should be considered, especially if chemotherapy is initiated. Use extreme caution if planning red blood cell transfusions as even one unit can cause devastating consequences. Patients are at risk of intracerebral hemorrhage.

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

From lung ca or CNS infection. Caused by release from ectopic sites such a lung neoplasm or from CNS infections. Clinically the patient is euvolemic with a less than maximally dilute urine and a urine sodium >30. Treat mild with water restriction and perhaps demeclocycline which produces a nephrogenic diabetes insipidus. The dose is 250 mg PO Q4. See the Hyponatremia chapter for information on the treatment of symptomatic presentations.

Hyperuricemia

renal failure. Rx or proph c allopurinol, alk of urine, fluids. Diamox 1 gram QD to further ralk urine. Mannitol if ¯ urine output.

Hypercalcemia

short QT. Hydrate, after adequate hydration give lasix, monitor k, May need HD. Calcitonin 4 units/kg subcut Q 12 Zometa 4 mg over 15 minutes or Pamidronate 60 mg for Ca <13.5 or 90 mg otherwise over 20 minutesand a for a week and a measles mumps and and   Can try bisphosphinates.

Neurologic Emergencies

Acute Spinal Cord Compression

back pain with possible lower extremity weakness, difficulty with ambulation, urinary sx (retention or incontinence) Get stat MRI even if previous are normal as compression fracture secondary to weakened bone can cause acute change. Give Dexamethasone, the patient will need to be admitted for radiation and possible laminectomy.

Cerebral Herniation

Uncal-lateral mass compresses brain stem. Unilateral blown pupil, ipsilateral paralysis. Central-downward compression of pons. B pinpoint. Tonsillar-posterior mass compresses cerebellum through foramen. Vomitting, LOC, Resp changes. Keep PaCO2 at 30, mannitol, steroids CNS Infxns Onc c AMS should get LP

Carcinomatous Meningitis

CT – and then + LP c 10-15 cc for cytology Carcinomatous meningitis is the diffuse involvement of leptomeninges by infiltrating malignant cells. Although uncommon, diffuse leptomeningeal metastases of extracranial tumors have been increasingly reported due to the improved survival of patients with systemic anti-neoplastic therapies, the availability of new diagnostic modalities, and rapid diagnosis and treatment. The most common primary malignancies associated with this condition include lung, breast, melanoma, and the lymphomas and leukemias. Signs and symptoms depend on which part of the neuroaxis is seeded. Cerebral involvement may present with headache, change in mental status, and persistent nausea and vomiting. Spinal cord involvement may present with weakness, paresthesias, and back pain. Cranial nerve involvement occurs in 50% of patients, manifested as diplopia, decreased visual acuity, hearing loss, and facial numbness. A brain imaging study should be performed before LP. MRI is the preferred imaging study, but in most EDs it is often not readily available. If MRI is not immediately available, a cranial CT scan with IV contrast should be performed before LP. Abnormalities include hydrocephalus and contrast enhancement, which may be focal or diffuse and may have either a smooth or nodular contour. However, the contrast-enhanced CT scan may be normal in up to 44% of patients with carcinomatous meningitis. Identification of malignant cells in the CSF is diagnostic, although initial tests may be falsely negative in up to 50% of patients with carcinomatous meningitis. At least 5-10 cc should be drawn for cytology, and serial LPs may be required to confirm the diagnosis. If the classic but nonspecific findings of increased opening pressure, moderate to extremely low glucose, elevated protein, and pleocytosis are found, a presumptive diagnosis can be made. Contrast enhanced MRI has an important ancillary role for imaging in suspected leptomeningeal tumor, especially in cases in which LP is contraindicated or in which CSF examination is equivocal. It is also used to monitor response to therapy in patients with known leptomeningeal disease. Multiple studies, however, show a false negative rate of approximately 30%. Because the entire neuroaxis may be involved, treatment consists of immediate intrathecal chemotherapy and external beam radiation. In general, fixed neurologic deficits, such as cranial nerve palsies or paraplegia, do not resolve with therapy. The median survival of solid tumor carcinomatous meningitis is 2-3 months whereas untreated patients or nonresponders have a median survival of 6 weeks. Given the prognostic implications of diagnosing carcinomatous meningitis, the possible need for multiple LPs to make the diagnosis, and the prolonged survival associated with appropriate therapy, most patients with nondiagnostic LPs and cranial CT scan results should be considered for admission to the hospital with repeat LP and MRI evaluation. (Source Unknown)

Pancoast Tumor (Superior Sulcus Tumor)

Apical lung Ca accounts for 3-4% of lung tumors. Presents as shoulder pain, C8 radiculopathy, Horner’s syndrome, or atrophy of hand muscles. If an older person presents with a C8, get the C-XR.

Hodgkin’s Disease

3-5% will present with pain upon drinking alcohol. It may be in the areas of lymphadenopathy or in the bones, particularly the spine and the pelvis. Another odd presentation is pruritis; this diagnosis should be considered in any young person with unexplained pruritis. Also in young people that present with shingles.

Multiple Myeloma

In this plasma cell malignancy, the patient will present with anemia, bone pain, hypercalcemia, and lytic bone lesions. A clue to the diagnosis may be a low anion gap. A anion gap <3 is usually abnormal. Depending on the lab normal may be 12 +/- 4 or 6 +/- 3. Other causes of low anion gap include lithium, hypoalbuminemia or elevations of normal cations.

Adrenal Insufficiency

     

Neutropenic Enterocolitis

Necrotizing enterocolitis (typhlitis) in adults Louis-Michel Wong Kee Song, MD, FRCP(C) Norman E Marcon, MD, FRCP(C) UpToDate performs a continuous review of over 350 journals and other resources. Updates are added as important new information is published. The literature review for version 14.1 is current through December 2005; this topic was last changed on August 8, 2005. The next version of UpToDate (14.2) will be released in June 2006. INTRODUCTION — Typhlitis (from the Greek word “typhlon,” or cecum) is a life-threatening, necrotizing enterocolitis occurring primarily in immunosuppressed patients. It is synonymous with “neutropenic enterocolitis” and “ileocecal syndrome.” Typhlitis was originally reported in children who underwent induction chemotherapy for acute leukemia [1]. It has subsequently been described in children or adults with acute myeloid leukemia, multiple myeloma, myelodysplastic syndromes, aplastic anemia, acquired immunodeficiency syndrome, cyclic or drug-induced neutropenia, and after immunosuppressive therapy for solid malignancies and transplants [2-6]. (See “Complications of acute myeloid leukemia”). Rare reports have described it in otherwise healthy adults following ingestion of food contaminated with C. perfringens type A [7]. The true incidence of this disease is unknown, but typhlitis has been reported to be present in up to 46 percent of childhood leukemia cases at autopsy [2,8]. PATHOGENESIS — The pathogenesis of typhlitis is incompletely understood. It probably involves a combination of factors, including mucosal injury by cytotoxic drugs or other means, profound neutropenia, and impaired host defense to invasion by microorganisms [4]. The microbial infection leads to necrosis of various layers of the bowel wall. The cecum is almost always affected, and the process often extends into the ascending colon and terminal ileum [2]. The predilection for the cecum is possibly related to its distensibility and its diminished vascularization relative to the rest of the colon. Gross and histologic examinations may reveal bowel wall thickening, discrete or confluent ulcers, mucosal loss, intramural edema, hemorrhage, and necrosis. Various bacterial and/or fungal organisms, including Gram negative rods, Gram positive cocci, anaerobes (eg, Clostridium septicum), and Candida sp., are often seen infiltrating the bowel wall. Polymicrobial infection is frequent. Only rarely are inflammatory or leukemic infiltrates identified [2]. Bacteremia or fungemia is also common, usually with enteric organisms such as Pseudomonas or yeasts such as Candida. CLINICAL MANIFESTATIONS — Typhlitis must be considered in the differential diagnosis of any profoundly neutropenic patient (absolute neutrophil count <500/µL), who presents with fever and abdominal pain, usually in the right lower quadrant. Symptoms often appear 10 to 14 days after cytotoxic chemotherapy, at a time when neutropenia is most profound and the patient is febrile [9]. Additional symptoms may include abdominal distension, nausea, vomiting, and watery or bloody diarrhea [2,8]. Peritoneal signs and shock suggest the possibility of bowel wall perforation. Stomatitis and pharyngitis, suggesting the presence of widespread mucositis, may be present. DIAGNOSIS — Typhlitis is usually diagnosed by characteristic ultrasound or CT findings in high-risk patients. CT is the preferred diagnostic modality since it appears to have a lower false-negative rate of diagnosis (15 percent) than does US (23 percent) or plain abdominal films (48 percent) [10]. All modalities indicate the presence of a fluid-filled, dilated, and distended cecum. Findings on CT may include diffuse cecal wall thickening; presence of intramural edema, air, or hemorrhage; localized perforation with free air; or soft tissue mass suggesting abscess formation. CT is usually helpful in the differentiation of typhlitis from appendicitis, appendiceal abscess, or even pseudomembranous colitis [11]. Typhlitis mimics acute appendicitis, and distinguishing between the two is important due to their different management [12]. Acute lower gastrointestinal bleeding, which occurred in 35 percent of typhlitis cases in one series, should suggest typhlitis instead of appendicitis [2]. Other diagnoses to consider include pseudomembranous colitis, ischemic colitis, and Ogilvie’s syndrome (colonic pseudo-obstruction) [11]. Blood and stool cultures and C. difficile toxin assays should be performed. Plain films of the abdomen are nonspecific but, occasionally, a fluid-filled, distended cecum with dilated adjacent small bowel loops, thumbprinting, or localized pneumatosis intestinalis is seen (show radiograph) [8]. In a stable patient with possible typhlitis without an indication for an emergency laparotomy, a diagnostic laparoscopy can be considered when the diagnosis remains in doubt despite cross-sectional CT imaging [4]. Barium enema is hazardous in the presence of potentially necrotic bowel, since it can cause perforation [13]. Similarly, colonoscopy is relatively contraindicated in the presence of neutropenia and thrombocytopenia, and air insufflation may precipitate cecal perforation. However, it may be reasonable to perform a flexible sigmoidoscopy with gentle manipulation and air insufflation if pseudomembranous colitis is suspected, although a sigmoidoscopy may be negative despite the presence of infection since pseudomembranes confined to the cecum have been described in neutropenic cancer patients with C. difficile infection. In those very few patients who underwent colonoscopic examination, mucosal irregularity with nodularity, ulcerations, and hemorrhagic friability, as well as a mass-like lesion mimicking carcinoma have been described [14,15]. MANAGEMENT — A general approach to patients with typhlitis can be suggested, although care should be individualized (show algorithm). In patients without complicated typhlitis (ie, peritonitis, perforation or severe bleeding), nonsurgical management with bowel rest, nasogastric suction, intravenous fluids, nutritional support, and broad-spectrum antibiotics is a reasonable initial approach [10,13]. Antibiotic coverage for C. difficile should be added if pseudomembranous colitis has not been excluded. Since fungemia and fungal invasion of the bowel can occur, amphotericin B or fluconazole should be started in neutropenic patients with protracted fever (>72 hours) despite broad-spectrum antibiotics. (See “Fever in the neutropenic adult patient with cancer”). Anticholinergic, antidiarrheal, and opioid agents should be avoided since they may aggravate ileus. An attempt to accelerate leukocyte recovery with granulocyte colony stimulating factor (G-CSF) is reasonable, since normalization of the leukocyte count may permit containment and healing of bowel lesions [3,8,16]. Other possible treatments such as selective decontamination of the digestive tract, enteral nutrition (for maintaining structural and functional integrity of the gut), glutamine (for maintaining gut integrity and local and systemic immune function), and granulocyte transfusions as means of reducing the incidence or duration of typhlitis are of unproven benefit but deserve further study [4,17]. Surgical intervention is recommended for those with peritonitis, free perforation, persistent gastrointestinal bleeding despite correction of coagulopathy and cytopenias, or clinical deterioration during close observation and serial examinations [8]. If surgery is performed, a two-stage right hemicolectomy is the preferred approach, and further chemotherapy should be delayed until recovery. A surgeon may be tempted not to resect edematous bowel without apparent severe inflammation or gangrene. The caveat is that diffuse mucosal necrosis may be present underneath unimpressive serosal inflammation [4]; incomplete removal of all necrotic tissue uniformly results in death. Patients developing typhlitis during chemotherapy are prone to develop this complication again during subsequent treatments. Sufficient time should be allowed for complete healing. In addition, bowel decontamination has been suggested before resumption of chemotherapy. PROGNOSIS — Initial reports of patients with typhlitis described mortality rates between 40 to 50 percent, with most deaths attributed to transmural bowel necrosis, perforation, and sepsis. More recently, early recognition and progress in management have probably reduced mortality, although no large series have been published.           | | |