“Facts are stubborn, but statistics are more pliable.” -- Mark Twain Alan Chan, MD Med-peds PGY4 Z A CD Chief Complaint: weakness HPI: 46 yo Caus woman reports to the ER after “fall onto tailbone” a couple days prior to presentation. Had presented initially after fall and diagnosed with “back sprain” and sent home with supportive care and pain medications. Now getting progressively weak, but moreso over past day. Difficult to walk and brought in via EMS on stretcher. Difficult to urinate (has to “push?”) and has not today yet. Also developing subjective fever today. Severe pain and more localized on neck area. Dysphagia and some odynophagia. No chills, no N/V. Headache x couple times. Some sore throat x couple weeks, non productive cough. No dyspnea on exertion. No sick contacts. No weight loss. LMP last week. Z A CD Medications • Flexeril 10 mg q8h prn pain • Lortab 7.5/500 q6h prn pain Z A CD Allergies NKDA PMH: none PSH: none ROS: No chills, fatigue, night sweats. No trauma, vision changes No rhinorrhea, sneezing; No dyspnea on exertion, edema, no shortness of breath, wheeze No recent illness Z A CD SH: Bookkeeper. 1 ppd x > 30 yr. Occasional EtOH. Patient denies IVDU FH: DM Z A CD VS in ER: Temp 102.5, Resp 24, BP 115/61, Pulse 152. 94% on 4L NC General: Alert female appears older than stated age and in acute distress due to back pain. HEENT: EOMI, PERRL, no scleral changes. OP clear with no intact dentition, dry mucus membranes. Red tongue. Neck: soft, supple, no LAP but difficult due to pain. Mild erythema along neck SCM. Chest: CTA bilat, no wheezing; poor air entry effort Z A CD CVS: tachy regular rhythm S1, S2, no murmur Abd: BS +, non TTP. No guarding. Ext: no edema, 2+ pulses Neuro: CN 2-12 intact, no tested deficits. 4/5 strength with intact reflexes at knee, elbow. Decreased light touch per patient. Skin: right antecubital area suspicious looking Repeat exam by neurology a couple hours later. CN 2-12 intact; DTRs 1+ in left, none in right. Plantar upgoing bilat. Motor LUE 1/5, RUE 1+/5. UE bilat 1/5. lt touch intact. Z A CD Differential Diagnosis CC: back pain, weakness, fever HPI: 46 yo with PMH: none Exam Findings Several – fever, appearance, mouth, neck, tachy, declining neuro findings Z A CD Laboratory Data CBC BMP Urinalysis Cardiac Enzymes Liver Function Tests Coagulation Endocrinology Serology Immunologic Studies Other Serology Body Fluid Analysis Cytology Pathology Z A CD Microbiology CXR EKG Ultrasound CT Scan MRI Other Studies Other Imaging Clinical Course Differential Diagnosis Discussion Please Press to Return Z A CD CBC 12.2 194 13.5 35 Seg Neutro 85, Lymph 3, Mono 4 MCV 84 (80-99) RDW 18.4 (<14.5) Z A CD BMP 134 107 11 3.9 19 0.7 AG 8 (3-15) Ca 6.5 (8.8-10.5) Mg 1.5 (1.8-2.5) PO4 xx (2.4-4.7) Z A CD 128 Urine Analysis color sp gr pH Hgb ketone glu prot LE nitrite urobil bili Z A CD yellow 1.025 5.5 mod sm neg 30 neg neg neg neg Microscopic 11-20 wbc 1-5 rbc UDS (got APAP and dilaudid) • Acetaminophen, opiates, THC, TCAa – pos • Methamphetamines, Barbs, BDZs, Cocaine, methadone, phencyclidine – neg Z A CD Cardiac Enzymes 1st - TnI 0.12 (0.08-0.5 increased risk); CK – MB 6.7 (0-6) CPK - 699 BNP – 177 2nd – 0.47 3rd – 0.39 Z A CD Liver Function Tests Z A CD AST ALT Alk Phos Albumin T Bilirubin D Bilirubin Protein 65 (15-41) 73 (7-35) 65 (32-91) 2.5 (3.5-4.8) 1.3 (0.3-1.2) xx (0.1-0.5) 5.6 (6.1-7.9) Lipase < 10 (18-51) Coagulation PTT PT INR Z A CD 24.5 (21-33) 11.4 (10.3-13.0) 1.0 Endocrinology TSH Free T4 Z A CD X (0.34-5.6) X (0.6-1.6) Serology • • • • • Z A CD HEPATITIS B SURFACE ANTIGEN Non-reactive HEP B CORE ANTIBODY IGM Non-reactive HEPATITIS A IGM Non-reactive HEPATITIS C ANTIBODY Reactive ! Genotype 3 Studies from abscess fluid Z A CD Cytology Z A CD Other Serology • Inflammatory markers – would have been very elevated Z A CD Body Fluid Analysis • AFB neg • X2 • Fungal neg • Mycology neg • MRSA tissue Z A CD Microbiology • UCx neg • BCx GPC MRSA!! Z A CD Z A CD • • • • • • • • • • • • • • • • Z A CD Chest X-ray 0755 8/20 FINDINGS: Lungs: Low lung volume. Bilateral lower lobe subsegmental atelectasis. Multifocal bilateral nodular and masslike consolidations predominantly in the lung periphery with a dominant lesion in the right upper lung zone. The etiology of these findings is indeterminate. Multicentric primary pulmonary neoplasia should also be considered. Multifocal pulmonary infection including septic emboli and opportunistic infections cannot be excluded. Pleura: Small bilateral pleural effusions. No pneumothorax. Heart and Mediastinum: Cardiomegaly. Tortuosity of the thoracic aorta. Abnormal contour of the mediastinum consistent with mediastinal lymphadenopathy. IMPRESSION: 1. Low lung volumes. Basilar atelectasis. 2. Multifocal nodular and masslike consolidations as described above. The differential diagnosis includes multicentric neoplasia (including metastatic disease) and multicentric infection (including septic emboli). 3. Small bilateral pleural effusions. 4. Mediastinal lymphadenopathy. Z A CD • • • • • Z A CD HR 143, PR 128, QTc 414 Sinus tachycardia Probable left atrial abnormality Borderline low voltage in frontal leads RSR’ pattern in V1 or V2, right RVH Z A CD CT neck soft tissue IMPRESSION: 1. Soft tissue swelling of the retropharyngeal and perivertebral space, and thickening of right sternocleidomastoid muscle with induration of surrounding fat, likely cellulitis versus phlegmon. There is thickening of the right sternocleidomastoid muscle, and induration of the surrounding fat, which could indicate early inflammatory changes. There is focal collection of fluid in the retropharengeal space and around the posterior muscles. It is unclear which space the fluid is in or whether some of it is phlegmon. 2. Right apical lung infiltration, most likely septic emboli. Z A CD Z A CD Z A CD MRI – C - SPINE without contrast • Impression: • Degenerative changes of the cervical spine with disk protrusions at the C4-5, C5-6, C6-7 levels. This appears to displace but does not appear to compress the spinal cord. There is extensive edema throughout the soft tissues of the neck posteriorly. There is prevertebral soft tissue swelling. In the setting of trauma this may represent extensive muscle injury and prevertebral swelling. In the setting of infection this may represent phlegmon or abscess formation withint the soft tissues. Slightly enlarged upper and mid cervical portion of the spinal cord with possible cord edema. Possibility of prevertebral and paraspinous abscess. Recommend contrasted study. Z A CD 2-D Echocardiogram CONCLUSIONS: Normal left ventricular systolic function, with an estimated ejection fraction of 60%. Normal right ventricular dimensions and systolic function. No significant valvular abnormalities including vegetation. Normal pulmonary artery systolic pressure of 27 mm Hg. No pericardial effusion. No previous study available for comparison. Z A CD Other Imaging • MRI L and T spine done after emergent OR • Postsurgical changes at the cervicothoracic junction with incompletely evaluated marked soft tissue abnormality in the posterior paravertebral soft tissues. There is effacement of the cervicothoracic spinal cord with edematous changes and effacement of the CSF space. • No acute abnormality of the lumbar spine for enhanced MRI. No drainable fluid collection. Z A CD Clinical Course • Given 10 mg IV of decadron in the ER, 3L of NS bolus • Taken to the OR by Neurosurg • C3-T2 laminectomy and evacuation of epidural abscess • Positive BCx x 4 sets, none after 5 days of antibiotics, but persistently febrile. • Dx of spinal epidural abscess and Lemierre’s syndrome. Z A CD Discussion - Goals • Overview of spinal epidural abscess (much more common than intracranial), retropharyngeal abscess (and other deep neck infections), Lemierre’s syndrome (postanginal sepsis syndrome) • Presentation, dx, and tx of each. MKSAP Q? Z A CD Overview – spinal epidural abscess • Doubled over past decades to 1 in 10000 hospital admits. • Risk factors include age, spinal instrumentation, IV drug use. • Comorbid medical conditions – DM, alcoholism, HIV, spinal abnormality, trauma, tattooing, local or systemic infection source • Bacterial spread via contiguous or hematogenous dissemination. Z A CD Pathogens • Staph aureus – 2/3 cases since from skin flora • Staph epidermidis (post op from spinal procedures, glucocorticoid injections, catheters) • Gram negative - E. coli, Pseudomonas • Rarely – anaerobic, mycobacteria, fungi, parasites Z A CD Complications • • • • Z A CD Endocarditis Vertebral osteomyelitis Psoas muscle abscess Epidural infection leading to cord injury by compression or vascular occlusion from septic thrombophlebitis. Presentation and Staging system • Triad of back pain, fever, and neurologic deficits rarely present – except in our patient! • Stage 1 – back pain at level of affected spine • Stage 2 – nerve root pain radiating from affected spine • Stage 3 – motor weakness, sensory deficits, bladder +/- bowel dysfunction • Stage 4 - paralysis Z A CD Diagnosis • • • • Clinical findings with labs and imaging Leukocytosis in 2/3, elevated inflammatory markers Bacteremia in about 2/3 as well, moreso in S. aureus Lumbar puncture is not routinely recommended unless myelography is done. Slight risk of meningitis or subdural infection if needle crosses the epidural abscess. Little additional info gained. • MRI recommended • Commonly misdiagnosed given nonspecific features on initial presentation. Z A CD XR – L3-4 narrowing CT – bony erosion of L3 and L4 Bone scan – inc technetium uptake MRI – abscess a/w osteomyelitis and diskitis Z A CD Treatment • Glucocorticoids to help swelling until surgery. • Surgery – decompressive laminectomy and incision and drainage and systemic antibiotics +/- removal of any implanted devices. • ABX – vanc, metro, cephalosporin 3rd or 4th gen x > 6 wk • Non surgical considerations – if patients refuses, high operative risk, paralysis over 24-36 hr, panspinal infection. BUT, may still require drainage and to control sepsis. • Preoperative neurologic stage is most important predictor of final neurologic outcome. • 5% mortality • Final neurologic outcome assessed at least 1 year out. • MRI in 4-6 wk or if clinical deterioration. Z A CD Neck space infections • Danger space is formed anteriorly by the alar fascia and posteriorly by the prevertebral fascia • Prevertebral space continues to psoas muscle • Can allow retropharyngeal infections to spread to mediastinum. Z A CD Quinsy aka peritonsillar abscess • All ages, but more in 15-30 years old • suppurative complication of acute tonsillitis with extension into the peritonsillar space. • Ill appearance with fever, sore throat, dysphagia, trismus (can’t open mouth), drooling, muffled voice • Usu GAS, occasional beta hemolytic strep, H flu, s aureus, anaerobes (unasys) Z A CD Parotits • Usually in more elderly population • Usu firm erythema with swelling of auricular areas. • Polymicrobial – S aureus and anaerobic; gram neg in hospitalized patients • OR viral – typically more prodromal period and bilaterally. Z A CD Submandibular space - Ludwig’s angina • Bilateral, BOTH submandibular and sublingual spaces, rapidly spreading cellulitis WITHOUT abscess or lymph involvment • 70-85% of cases follow infection of mandibular molar teeth • Can see enlarged tongue • Mouth pain, stiff neck, drooling, dysphagia. Symmetric swelling • Tx – AIRWAY!! – and also abx like unasys Z A CD Lemierre’s syndrome aka postanginal sepsis aka suppurative jugular thrombophlebitis • Venous thrombosis a/w inflammation in the setting of bacteremia • Usually preceded by pharyngitis or oropharyngeal infection. • Neck pain worse with turning away from involved side. • Dysphonia, dysphagia • Possible swelling and induration • Clinical manifestation of septic pulm emboli, persistent fevers despite antibiotics • Bugs – anaerobic like Bacteroides, or Fusobacterium Z A CD Hx and Tx • Described in 1936 with series of throat infections with anaerobic septicemia. • Increasing incidence, maybe by more reporting, increased antibiotic resistance, or better imaging studies. • Fusobacterium has had more PCN resistance. • Typically seen in previously healthy young adults. • Distant emboli from septic thrombophlebitis from jugular vein thrombosis – lungs, joints commonly affected. • Role of anticoagulation is controversal as segment of affected vessel is short. Z A CD Question of the Day Z A CD • 40 yo retired public health nurse with a 2 yr hx of rapidly progressive rheumatoid arthritis is evaluated prior to etanercept (enbrel). diclofenac, methotrexate, and prednisone all did NOT work. She had been in good health before developing rheumatoid arthritis. • PE is normal except for changes related to rheumatoid arthritis. CBC shows mild normochromic, normocytic anemia with normal leukocyte and platelet counts. A recent CXR was normal. • Which of the following tests would be most appropriate before starting therapy with etanercept? • • • • • A Nitroblue tetrazolium dye test B Measurement of quantitative serum immunoglobulins C Skin testing with mumps and Candida antigens D Tuberculin skin testing E Measurement of total hemolytic complement level (CH50) • D – TB skin test - this and other anti–tumor necrosis factor-α agents (e.g., infliximab/remicade and adalimumab/humira) are at higher risk for developing latent TB. • Patients with latent TB who do develop reactivation TB tend to present with extrapulmonary disease, and a quarter have disseminated disease. Active TB occurs within 12 weeks of beginning therapy with infliximab, 30 weeks of beginning therapy with adalimumab, and 46 weeks of beginning therapy with etanercept. Patients who have a positive screening test for latent TB should start isoniazid. Z A CD • CGD – def neutrophil fxn – check NBT dye test. • No humoral immunity – pulm inf’n, bacteremia, meningitis – check QuIgs • No cellular immunity – viral, fungi, intracell bugs – check TST, and mumps and candida antigen challenge • Terminal complement def – disseminated gonococcal or Neisseria meningitis – check CH50 • Even 5-10 mg pred increases inf’n a/w Cell medi immunity!! Patients taking anti–TNF-α inhibitors are at increased risk for developing latent TB. Patients about to begin therapy with anti–TNF-α inhibitors should undergo TST screening. Z A CD References • MKSAP 14 • Uptodate.com “Deep neck space infections”. Accessed 9/26/2010. • Emedicine article. “Retropharyngeal Abscess”, http://emedicine.medscape.com/article/995851-overview. Acessed 9/26/2010. • Darouiche, RO. Spinal Epidural Abscess. N Engl J Med 2006; 355: 2012-20. • Karkos RD, et al. Lemierre’s Syndrome: A Systematic Review. Laryngoscope 2009; 119: 1552-59. Z A CD Z A CD The future of telemedicine…