Cardiovascular Pathology Case 2

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Data for Case

Part 1

The patient is a 46 year old male who presented on 12-7-02 with a painful purple big toe. He also has pain in his right forearm and hand in an ulnar distribution, and notes that his fingers, turn white in the cold. They became very numb and then improve on rewarming.

His past medical history is significant for a two year history of abdominal pain which was believed to be caused by his gall bladder but after cholecystectomy the symptoms persisted. The pain was constant, dull and made worse with eating. He was diagnosed with ischemic bowel disease and referred to surgery. A 12" segment of small bowel was resected with placement of a gastrojejunostomy tube. Pathology of the bowel could not determine the etiology of the ischemia. A biopsy of his kidney showed arteriosclerosis and glomerulosclerosis with no immunologic staining patterns.

 

Review the History and Physical from 12-7-02.

A rheumatologist saw the patient on 12-9-02 and tests were ordered to identify the type of vasculitis.

 

1. What is your differential diagnosis?

 

2. What tests would you want to get?

 

3. What does an elevated sedimentation rate mean?

Part 2

The patient was subsequently diagnosed with vasculitis by muscle biopsy on 12-12-02 and continued to have worsening problems with patchy ischemia.Testing was negative for ANA, ANCA, RF and he was presumed to have poly arteritis nodosa (PAN). He was started on steroids and Cytoxan therapy for immunosuppression, but he continued to lose weight. Additional studies for vascular disease found that the patient was heterozygous for Factor V Leiden. He was admitted to the hospital on 8-16-03 with dry gangrene of the left great toe and severe abdominal pain.

Review the surgical pathology report on the muscle biopsy.

Review the admission history and physical from 8-16-03.

 

1. What is polyarteritis nodosa?

 

2. What additional risks does Factor V Leiden impose on this patient?

 

3. Review the EKG from this admission; are there any signs of cardiac ischemia?

 

 

4. An x-ray of the foot was performed to rule out osteomyelitis of the great toe, do you see any bone loss?

 

Part 3

 

His clinical labs on admission were consistent with his state of immunosuppression and infection. The patient was treated with surgical resection of ischemic bowel on 8-18-03 when free air was found on abdominal films.Pathologic review of the surgical material did not find evidence for active PAN.The patient developed fevers on the second postoperative day and it was thought that he had developed an anastomotic leak in the bowel and sepsis.He was given comfort measures and died on 8-21-03. An Autopsy was requested.

 

Review the labs at the time of death.

Sedimentation rate trends might help you.

Review the death summary.

Review the abdominal and chest film reports from the 18th.

 

(Abdomen 8-18)††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† (CXR 8-18)

 

The patient developed respiratory symptoms on the last two days of life.Review the CXRís from the 19th through the 21st.

8-19-03

 

8-20-03

 

8-21-03

 

1. What do the CBC and smear findings have to do with the diagnosis of vasculitis?

 

2. What changes are seen on CXR?

Part 4

 

The autopsy revealed that the patient had developed pneumonia as the immediate cause of death despite negative pre-mortem cultures.Two additional areas of ulceration in the bowel were found and the surgical anastomotic site in the bowel was intact.

 

Review the autopsy report.

Review the tissues and slides and pay attention to the areas of ischemic change as shown in these images.

 

Cecum with ulcers:

 

Anastomotic site of bowel:

 

Mesenteric arteries with EVG stain to show elastica:

 

Necrotic left great toe and second toe:

 

Microscopic view of edge of toe ulcer:

 

Kidney with marked deformity from multiple infarctions:

 

Renal arteries:

 

Coronary arteries:

 

Heart:

 

Aorta with minimal atherosclerotic change and kidneys:

 

1. Are the autopsy findings consistent with Polyarteritis Nodosa?

 

2. What vessels are involved in this disorder?

††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††

3. What other vasculitides may present like this?

 

Part 5

Assignment for next week

Using all of the information you have gathered from the chart, prepare a presentation about this case as you would for attending rounds with a concise summary of the history, physical findings, labs and x-rays. Your presentation should be about 5 minutes long. A copy of your presentation needs to be handed in to your facilitator by the end of the lab on 12/11/03.

Incorporate the following into your report:

1. Describe polyarteritis nodosa, its diagnosis and treatment.

 

2. Is atherosclerosis associated with vascular damage?

 

3. How does Factor V Leiden affect atherosclerosis?

 

4. Describe the etiology of ischemic infarcts of the tissues in this case

 

5. How does immunosuppression increase the risk of infection?

 

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DATA FOR CASE

 

Admission H&P 12-7-02

Rheumatology note 12-9-02

Surgical Pathology Report 12-12-02

Surgical Pathology Report 8-18-03

H&P 8-16-03

Operative Report 8-18-03

Clinical Laboratory Reports

Microbiology Reports

Sedimentation Rates Trend

Radiology reports††††††

Old CXR 12-7-02 for comparison

Death Summary

Autopsy Report

Normal Values

 

 

 

Admission HP 12/07/2002

 

cc: excruciating left big toe pain

HPI: This 46 year old male presents today with a painful purple left big toe present for the past 2 - 3 weeks. He has a history beginning about two years ago of some type of vascular problem. He began to have abdominal pain which was believed to be caused by his gall bladder since US showed some stones. It was resected but the patients symptoms still remained. The pain was constant and dull but was made much worse with eating or drinking. He suffered with this problem for several months and finally he was discovered to have ischemic bowel incidentally. He was immediately referred to surgery and had a 12" section of bowel surgically resected with placement of a GJ tube. The patient has never used the tube and tolerates his PO intake. At this time he was diagnosed with a vascular disease of unknown etiology. He went to numerous physicians in an attempt to figure out what may be causing this problem. He was sent to a rheumatologist who after significant testing decided that his problem was probably of a vascular not rheumatologic origin. He had a recent biopsy of his kidney done which showed arteriosclerosis and glomerulosclerosis but no immunologic staining patterns. He also continues to have attacks of abdominal pain the last of which was about one month ago and caused him to lose 10 pounds. The toe pain began about three weeks ago. The patient set up an appointment with a vascular surgeon for next Monday but could not tolerate the pain any longer when he reported to the emergency room this am. The patient describes getting pain as severe as a 10/10. He also reports that this intense pain causes purple blotches to appear and march up his legs but not to his buttocks. It blanches on pressing. The toe had caused some throbbing episodes occasionally in the past but nothing to this degree.

In addition, the pt. has this pain in his right forearm and hand in his ulnar distribution. He notes that his hand, mostly his fingers, turn white in the cold and become very numb but it improves when warming up. The pain is constant regardless of the temperature. The patient has had an extensive work-up for many different potential problems, but none of the results have been rewarding. The patient does report a history of livedo reticularis and possible palpable purpura. The patient had vascular surgery see him today but they decided that his toe problem was more of a vasculitis type problem and so rheumatology was consulted and has added a great deal to the assessment and plan of how we should treat and attempt to diagnose a problem in this patient.      

PMH: Pain in Ulnar nerve distribution in R arm from elbow to fingers - Past 1-2 wks
    HTN - Well controlled (120's to 130's ) with medication
    History of constipation causing rectal tears

PSH: 12" of small bowel (not duodenum) resected
    Kidney biopsy 10 years and 3 wks previous
    Cholecystectomy - 99

Meds: Lotensin 10 mg po bid
       HCTZ 12.5 mg po qhs
       Zocor 20 mg po qhs
       Percocet 7.5 mg po q4-6 hrs prn
       Niacin, Arginine, Folic Acid OTC supplements

Allergies: NKDA, Wheat allergy

FH: A brother has HTN and Hep.C
    Mother has hyperlipidemia, some kind of arthritis
    Sister may possibly have Raynaudís syndrome

SH: Married with one daughter who is in good health. Works as an airline mechanic. He has been exposed to all of the solvents and hazardous materials associated with that job. Pt. has had no history of smoking and has a distant history of alcohol use. He served in Desert Storm.

 

ROS:

HEENT: Denies SOB, mouth ulcerations, pain in the neck and nosebleeds as well. The pt. is bald but wears a hairpiece.
CV: The pt. denies CP, heart palpitations or racing.
Pulm: Denies lung problems or respiratory infections.
Abd: Has pain off an on. Currently is symptom free. No blood in stool.
GU: Has difficulty starting and stopping his urine stream.
Extrem: Pt. denies stiffness in joints or back pain. He has generalized full-body muscle aches.
Neuro: Denies loss of balance, vision, or memory
   
PE:

Vitals: T:36.3, HR:108 BP:115/80, RR:18 SpO2:99% on RA
General: Tired, cachectic man in noticeable discomfort
HEENT: TM's clear, PEERLA, EOMI, OP pink and moist, no hemorrhage or ulcerations, no lymphadenopathy, no thyromegaly, no carotid bruits, no JVD
PULM: Normal lung excursion, lungs CTA

CV: No heaves or thrills, nl S1/S2 no M/R/G detected
Abd: No masses, +BS, soft & non-tender, spleen tip palpated, hepatic border 2 cm below the costal ridge, no CVA tenderness. A GJ tube is present on his left side.
Extremities: no pulses palpated in DT or DP in either foot. Left big toe is exquisitely tender and purple on the medial side. The toe is also cold. There is pain in the ulnar distribution on his R. arm below the elbow. No petechia, ulcerations, or splinter hemorrhages detected.
Neuro: CN II-XII grossly intact, UES & LES 4/5, all reflexes intact, feet hypersensitive to stimuli, diminished vibratory sensation in LE.

 

Labs:

CBC: 7.5/10.3/30.2/483 %P-68.1, %L-17.7, %M-9.4, %E-3.9, %Ba-0.9  

BMP: 136/3.7/92/28/28/2.4/100 Ca-8.9 AG-16 Delta Gap-34

ESR: 50
UA: Sp grav-1.008, Protein-trace, Blood-Neg, Nit.-Neg    

Coags: PT-14.4, PTT-47, INR-1.1

CXR: No abnormalities detected. Clear chest

A/P: 46 y/o male with ischemic bowel problems and thrombosis of his left big toe.

1. Painful toe - The pt. is obviously suffering greatly from the entity causing the problem with his toe. He needs pain control and an aggressive work-up to determine the best way to treat this problem. This problem is most likely related to the problem causing his bowel ischemia, overall myalgias, and neuropathic pain. He best fits into the category of a medium vessel vasculitis with PAN topping the list. He demonstrates a chronic anemia, bowel ischemia, weight loss, myalgias, and signs of mononeuritis multiplex all of which fit with PAN. Hypertension, renal involvement, abdominal problems, cholecystitis, livedo reticularis, and palpable purpura are also features of this problem and this patient manifests them all. However, most of the time if PAN is untreated within 2 years it is fatal and this pt. has had problems for about this period of time.

Less likely moderate vessel vasculitides are Takayasu's or Viral induced infections. Cryoglobulinemia almost always occurs in conjunction with Hepatitis C and Hepatitis B will manifest itself much like PAN. Takayasu's is also possible except that there should be major aortic involvement and this has not been demonstrated. The pt. has never smoked and has had unilateral extremity involvement and began in the belly so Buerger's vasculitis is also unlikely.

The small vessel vasculitides are also a possibility for this man's problems. Wegner's, HSP, and mixed cryoglobulin vasculitis secondary to Hep B. or C are a possibility. His clinical picture does not fit this group as well as the medium vessel vascular inflammatory disorders, especially since this man has few cutaneous manifestations.   

An anti-phospholipid antibody syndrome may also be to blame for these problems. To be diagnosed with one of these syndromes there must be an actual event like thrombosis and either a positive anticardiolipin or lupus anti-coagulation test. Since the pt. has had a possible thrombotic event, these other two tests should be looked for to determine if he may have one of these conditions. The heparin drip he is on should protect him if he does have this condition. However, his clinical picture does not fit the signs and symptoms of these disorders very well but these causes must remain on the differential until some lab results can help rule in or out the specific problem. An elevated PTT is frequently found in pt's with either SLE or RA most often caused by lupus anti-coagulant.   

The plan is to order a huge spectrum of labs to try and figure out what is going on in this man. The justification for this is that he may have a life-threatening condition and delaying work-up could be dangerous for him.
- draw lupus anti-coagulant and anti-cardiolipin antibody levels
- draw Protein C, S, Factor V, and anti-thrombin levels
- draw homocysteine levels
- draw B2 glycoprotein abs.
- draw P-ANCA, C-ANCA
- draw cryoglobulins, CPK, and recheck RF and ANA
- CXR for poss granulomatous disease
- draw Hep. B and C serologies and draw LFT's
- Heparin to relieve symptoms
- PCA to help control the pain

2. CRI - The pt. has had a baseline creatinine of about 2 due to glomerulosclerosis. He is spilling some protein in his urine. It would be good to quantify exactly how much protein he is losing to help determine his specific problem. He does have a calculated anion gap, but this is likely due to his failing renal function not a true metabolic acidosis
- 24 hour urine for protein

3. Increased SED rate - This is a very non-specific test but it has remained elevated for a long time. It certainly leads down the road to considering a connective tissue cause of vasculitis.

4. Ischemic Bowel - As mentioned above, this is most likely due to the same cause as the pt.'s toe pain. He continues to have pain on and off and products with wheat flour appear to make this worse. He is tolerating po intake just fine at this time. Therefore, we will give him a wheat free diet
- Wheat free diet

5. Wt. loss - This has occurred secondary to times when #4 above has been a problem. The pt. has been recently gaining weight since he has felt like eating. We will feed him whatever he can tolerate.

6. Anemia - It is unclear at this point why this pt. had this microcytic anemia. Some of the vasculitic syndromes are associated with anemia. His failing kidney function may also have something to do with this. We will get some labs to see where the etiology of this problem may be.
- Fe studies including total iron, ferritin, TIBC, etc.
- reticulocyte count
- peripheral smear

7. Elevated PTT - As mentioned in #1, an elevated PTT not related to being anticoagulated may be related to some rheumatologic conditions. The patient has had and elevated PTT before starting heparin therefore using PTT to determine heparin dosing is difficult. However, heparin levels themselves can be measured and should be done in this case. The normal range is 0.35-0.75.
- d/c PTT for following heparin
- begin using serum heparin levels to follow anticoagulation

8. Neuropathy - The pt. complains of neuropathies in his feet and his right hand. He is hypersensitive to stimulation on the bottom of his feet and complains of intermittent tingling and pain. He should have nerve conduction studies done to locate the best location to obtain a biopsy. Vessels where the neuropathy is a problem will most likely have the pathology that will be diagnostic.
- Nerve conduction studies

9. Cardiac - This is probably not a cardiac problem but there may be some endocarditis that is causing this. The BP has been well controlled on his current medications and those should be continued. Homocysteine can cause heart problems and it should be rechecked to make sure it isn't involved in this problem. It is still not clear and in fact it is unlikely that he actually has atherosclerosis. However, if he does cholesterol emboli could cause this problem. His previous records indicate a very good LDL and cholesterol level and that he was put on a statin more for hope it would have some effect than for a clinical need.
- continue Lotensin
- EHCO to check for endocarditis
- draw homocysteine levels
- continue Zocor 20 mg po q.h.s. for now

10. Rectal tears - The pt. states that he has had recent tears in his rectum since having some increased hardness of his stools. He is very afraid to have narcotic treatment without keeping his stools soft. We will give him an aggressive regimen with his PCA.
- docusate 100 mg po bid
- Senna 17.2 mg po bid

11. Prophylaxis - The pt. is anticoagulated with his heparin so DVT's are not a concern, but the pt. does have a history of esophagitis so he should get an H2 blocker while an inpatient to avoid reflux.
- Ranitidine 300 mg po qd

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Consultation Note12-9-02

 

Rheumatology Consultation follow-up

46 yo male admitted with ischemic toe

Today: toe pain perhaps better -- on pain meds
       no abdominal pain, no n/v, good appetite
       recurring blotchy rash on legs
       persistent dysesthesias of forearm

MEDS: Benazepril, Docusate, Gabapentin, HCTZ, Ranitidine, Simvastatin, Warfarin, Narcotics per pain service, Heparin

Exam: afebrile, 97-110, 18, 103-140/70's
General: cachectic
HEENT: white sclera, no oral lesions
Chest: clear
CV: Regular, no murmurs/gallops
Abd: BS+, soft, mildly tender with light touch of skin, J tube in place
Ext: no pitting
MS: hands/wrists/elbows/knees/ankles/mtp's -- no synovitis
SKIN: + lower extremity livido today, left toe is warmer, +ecchymotic/mottled changes medially - unchanged, spooning of nails
Neuro: dysesthesia -- right ulnar forearm and 4th and 5th digits, motor
grossly normal in this distribution, nl light touch of lower extremity

Labs over past 1.5 years: nl porphyria evaluation, sl elevated homocysteine,
negative Celiac sprue eval, neg Whipple's bx, ANCA negative, RF neg, ANA
neg, persistently elevated ESR's
Kidney Bx 11/01 -- arteriosclerosis/glomerulosclerosis

Labs on admit wbc 7500, hct 30, plt 483
       creatinine 2.4 (up from 1.8 last)
       U/A -- no protein, no blood
   ††† PTT 49
       ESR 50
   ††† ANCA negative

Subsequent labs: nl liver tests, nl CK, RF neg, hep B neg

A/P: 46 yo male with the following problem list:
*Ischemic digit -- plethysmography showing diffuse bilateral small vessel diminished blood flow.
*Elevated PTT -- no 1:1 or Lupus AC has been done yet!
*Suggestion of inflammation --
    high ESR (but renal insufficiency may falsely elevate)
    high Plts
*Anemia - low Fe, low Transferrin, Ferritin 218, reticulocytes 1.1%
    consistent with AOCD, no Fe deficiency with ferritin > 100
*Renal insufficiency - bland U/A with recent bx showing arteriosclerosis only
*Ulnar Dysesthesias/Paresthesias with apparent motor abnormality
*Hx Ischemic Bowel - bx in 2001 showing no active inflammation/vasculitis
    We do not have the mesenteric angiogram which was apparently done then.
*Cachexia
*Livido Reticularis
*Myalgias
*Raynaud's

Still, the two most concerning diagnoses include systemic vasculitis, particularly PAN, and antiphospholipid antibody syndrome (APS). Since admit, we still do not have a better handle on the diagnosis, awaiting multiple labs, an ECHO, and nerve conduction studies. Fortunately, his condition remains stable with his toe perhaps even mildly improved. I am not convinced that we currently have proof of active inflammation and

Systemic vasculitis -clearly compelling clinical picture--however, ESR and Plt elevation alone, especially with renal insufficiency, will not be sufficient to warrant therapy. Hence, we need to continue to look for other vasculitis mimics and look for a good source of tissue to document active inflammation. He has had at least 1.5 years of sx's without prednisone or cytotoxic treatment. This alone speaks against active vasculitis throughout this time. Alternatively, he may have had active inflammation in the past and be suffering now from complications of chronic endothelial damage/repair -- atherosclerotic-like changes and endothelial dysfunction/Raynaud's.

Recommendations are unchanged from 12/7 consult.

RECOMMEND:
Await:
    Anticardiolipin Abs
    Lupus Anticoagulant Panel
    Hypercoagulable eval -- Pro C/S, FV Leiden
Please get "CBC with manual diff" to look at RBC morphology and to look for eosinophilia as seen in cholesterol emboli, get daily HCT on Heparin too
ECHO -- looking for vegetations/atrial myxoma
24 hour urine -- creatinine and protein and SPEP/UPEP
Nerve conduction studies for ulnar dysesthesias
Please obtain old mesenteric angiogram. May consider repeat mesenteric angiogram here if no apparent bx site.

Repeat chem 7 -- ? acute change in renal function
Check Lactate (sl elevated AG on admit, hx ischemic bowel, cold toe)
Guaiac stools

TREATMENTS:
Continue Heparin (no enoxaparin due to renal insufficiency)
Would hold off on Coumadin until we know if bx or arterial stick for angiogram may be pursued.
With hx of "Raynaud's" and abnl plethysmography, could add Nifedipine for improved perfusion.

 

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Anatomic Pathology Report 08/18/03 SMALL BOWEL RESECTION

SP CLINICAL HISTORY

Abdominal pain and distention

SP GROSS DESCRIPTION

Container one labeled "ileum" contains a segment of small intestine, 18.5 cm in length x 2.0 to 3.0 cm in diameter. Much of the central 12.0 cm is covered with thick, geographic, purulent, yellow-white exudate, with focal hemorrhage and patchy, more fibrinous or fibrous serosal adhesions. There is a modest wedge of mesentery, variable smooth and glistening, but on one side also showing fairly extensive geographic exudate. A fresh silk suture marks a transmural perforation measuring 5 x 2 mm, that on opening the duct is at the base of a sharply punched out mucosal ulcer, 1.0 x 0.7 cm. The mucosa otherwise is mostly relatively normal in appearance with a just a very vague, inconspicuous, pink to light violaceous mottling. Scattered about the mucosa are multiple small inconspicuous shallow erosions or ulcers measuring 1-5 mm. 5.0 cm from one end either is a 2.5 cm segment of slight serosal thickening and luminal narrowing. 1A-1B - surgical margins, inked, each including punctate and slightly larger but small shallow mucosal erosions; 1C - sections of the largest mucosal ulcer with sutured transmural perforation; 1D-1E - random sections including small and punctate mucosal erosions; 1F-1L -generous sections of mesentery with major mesenteric blood vessels.
Container two labeled "jejunum" contains a segment of small gut measuring 45.0cm in length x up to approximately 3.3 cm in general average diameter. The serosal appearance is variable, from smooth to shiny to dull and slightly granular, to showing geographic areas of layered, thick, yellowish, gray-white exudate, and scattered areas of serosal hemorrhage and fairly delicate serosal adhesions. Approximately 12.0 cm from one surgical margin, there is a 5.0 cm segment of slightly bulbous dilatation and thinning of the wall, associated with a small, slight, band-like stricture and contracture of the mesentery and slightly onto the adjacent gut wall. There are two freshly sutured, transmural perforations, one 3.5 cm from one surgical margin, the second 2.5 cm from the opposite surgical margin, both associated with either geographic exudate on the serosal surface or a surrounding rim of gray-green apparent necrosis of the serosa and muscular wall. The opened segment shows a variable mucosa, in some areas normal, larger areas showing a slight darker, violaceous to red maroon discoloration. In the dilated thin-walled area, the mucosa shows a variable appearance with some flattening and granularity, surrounding very irregular, somewhat serpiginous areas of shallow mucosal ulceration measuring up to 3.0 x 1.0 cm, generally somewhat linear. Several small scattered superficial mucosal erosions from punctate up to 5 mm are identified. Both transmural perforations are associated with punched out, full thickness mucosal ulcers measuring up to 5-7 x 2-4 mm. 2A - one surgical margin; 2B - perforation near the surgical margin; 2C - opposite surgical margin; 2D - perforation near this margin; 2E-2F - sections of the dilated area with the large mucosal ulcers; 2G-2H - random mucosal sections trying to demonstrate the punctate and small mucosal erosions; 2I-2L - sections from mesentery.

 

SP MICROSCOPIC EXAMINATION

Sections of the ileum show small intestine with mucosal ulceration and perforations. The margins show mesenteric inflammation but viable tissue. Sections of the jejunum also show small bowel with areas of ischemic necrosis and perforation. The surgical margins show mesenteric acute and chronic inflammation but show viable tissue. Sections of the mesentery of both specimens show numerous vessels with evidence of old vasculitis. This includes disruption of the internal elastic lamina, mural fibrosis and thrombosis with recanalization. We do not see evidence of acute vasculitis and these changes would be that of healed polyarteritis nodosa. These changes
occur in multiple medium-sized vessels.

 

SP DIAGNOSIS

1. ILEUM, PARTIAL EXCISION -
- MUCOSAL ULCERATION AND PERFORATION.
- MESENTERIC VESSELS WITH EVIDENCE OF OLD VASCULITIS.

2. JEJUNUM, PARTIAL EXCISION -
- ISCHEMIC NECROSIS.
- PERFORATION.
- MESENTERIC VESSELS WITH EVIDENCE OF OLD VASCULITIS.

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Anatomic Pathology Report 12-21-02 MUSCLE BIOPSY

SP CLINICAL HISTORY

Not provided.

SP GROSS DESCRIPTION
Received labeled with the patient's name, medical record number and "muscle" is fresh tissue measuring 
1.5 x 1.0 x 0.3 cm. The specimen is divided into four portions. One piece of tissue is placed in glutaraldehyde 
and saved for possible electron microscopy. Two pieces of tissue are frozen and submitted for histochemical 
staining. One piece of tissue is placed in formalin and submitted for light microscopy. The formalin fixed 
tissue consists of a 2.1 x 0.7 x 0.5 cm, tan-brown, ragged, fibrous soft tissue. 
Received labeled with the patient's name, medical record number and "nerve" is fresh tissue that measures 
2.0 x 0.2 x 0.2 cm. The specimen is divided into two portions. One piece of tissue is placed in glutaraldehyde 
and sent for plastic embedding and thick sections. One piece of tissue is placed in formalin and submitted 
for light microscopy. The formalin fixed tissue consists of a single tan-white, smooth, fibrous soft 
tissue measuring 1.4 x 0.2 x 0.2 cm. Toto 1A with instructions to histology for cross and longitudinal sections.
 
SP MICROSCOPIC EXAMINATION

The histochemical stains on the frozen tissue demonstrate skeletal muscle with scattered atrophic fibers. There is no inflammation. There is no degeneration or regeneration in the fibers. The vessels appear normal. The ATPase pH 9.4 shows that the atrophic fibers are Type II fibers. The normal mosaic pattern of Type I and Type II fibers is seen. There is no evidence for a neurogenic atrophy. The modified Gomori trichrome shows the normal fiber architecture. The NADH shows the normal inter myofibrillar architecture. The PAS shows no excessive glycogen. The paraffin embedded section of muscle demonstrates two arterioles with chronic inflammatory cells infiltrating the walls. There is eccentric involvement of the vessel wall in one of the vessels. There is no necrosis of the vessel walls. The inflammation is primarily composed of lymphocytes. The paraffin embedded section of nerve demonstrates several arterioles with perivascular cuffing by lymphocytes and involvement of the vessel walls by the inflammation. There is no overt necrosis of the vessel walls.

 

SP DIAGNOSIS

1. GASTROCNEMIUS MUSCLE, BIOPSY, SKELETAL MUSCLE WITH VASCULITIS

2. NERVE, BIOPSY, PERIPHERAL NERVE WITH VASCULITIS AND FOCAL LOSS OF MYELINATED FIBERS

 

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History and Physical8-16-03


HPI: This is a 46 yo white male with PAN (negative HBV and HCV studies, + mesenteric angiogram, mononeuritis + bx, ischemic toes, ischemic bowel/resection) dx 12/01, has been on steroids and Cytoxan subsequently with persistent active inflammation. He has necrotic toes which require amputation, and he has malabsorption issues with + fecal fat studies, in need of subsequent GI evaluation.

Yesterday, seen by rheumatology, who noted persistent evidence of inflammation with ESR 82 and new vasculitic-appearing leg ulcer as well as persistent wt loss. Due to concerns of malabsorption, plans for high dose Solu-Medrol X 2 days with increase of prednisone to 100 mg qd were made.

Today, while pt was here to receive his 2nd Solu-Medrol infusion, pt complained of severe abdominal pain that started that am, which he describes as a cramping feeling. He says this pain varies in intensity from 10/10 at its worst to a 4/10 at its best. Despite this pain he sates his appetite is okay. He denies any nausea or vomiting. 2 year history of chronic diarrhea, with no recent change in its character. Denies any BRBPR or melena. He states he has episodes similar to this about one time a month, with resolution after rehydrating.

PMH:
1) PAD dx 12/01. Course as outlined above
2) ischemic bowel with resection of small bowel 12/00
3) Dry gangrene of L great and second toe.
4) HTN
5) jejunostomy tube
6) cholecystectomy

Meds:
Cytoxan 150 mg qd
Prednisone 40 mg qd
Neurontin 300 mg bid-tid
Lotensin 10 mg bid
Fentanyl patch 50 mcg
Elavil 50 mg bid
Nifedipine 30 mg qd
Pancrease 3 cap tid, and amylase and lipase
Zantac 150 mg bid prn
Coumadin 3 mg qd
Zocor 20 mg qd--last lipids very low so he is holding
Actonel 30 mg q week
Bactrim DS 1 po q mwf
Percocet 7.5 mg qd to bid

Allergy:
NKDA, Wheat intolerance

FH: Mother has hypercholesterolemia and arthritis. Sister has Raynaud's phenomenon.

SH: He is married with one daughter. No tobacco. No alcohol. No IVDA.

ROS: No fevers, + chills, + weight loss, no change in appetite, o rash, no bruising, no HA, no dizziness, no syncope, no vertigo, no tinnitus no cough, no dyspnea, + palpitations, no CP, + difficulty swallowing ("food gets stuck"), no heartburn, no N/v, no dysuria, nocturia (1x per hour), + numbness. + body aches.

EXAM: 93    140/82    16    35.4
HEENT: PERRLA, EOMI, no icterus noted. OP clear. Eschar present over L eye.
Neck: No TM, ? of supraclavicular lymph node on L vs vessel.
chest: CTAB
CV: rrr, no mrg
Abd: Soft, non distended, bilateral lower abdomen tenderness. Tender to percussion. No masses, no HSM. BS+.
Ext: Left great and second toe necrotic. L lat malleolus with ulcer. L should with black eschar. L elbow with eschar. R Achilles with eschar. R heal with eschar.
Musculoskeletal: hands/wrists/elbows/knees/ankles - no synovitis, nl rom, nontender bilaterally

LABS:
WBC 5.1 (72% PMN, Band 25, 2% lymph) HCT 25.3   Plt 379
Na 133   K 3.3    Cl 95    CO2 28    BUN 21    Cr 1.5   Glu 117
AST 12    ALT 15    Alk Phos 59   Alb 2.7   T bili 0.3
PT 28.5   INR 2.7   Lactate 5.9   Lipase 41    Amylase 36
ESR 82 (8/15/02)

Ab x-ray: Large amount of stool, no free air.

A/P:
1) Abdominal Pain: With past hx of mesenteric ischemia and elevated Lactate, concern for recurrent ischemia. However, pt reports exact same pain multiple times in past, resolves with hydration. Surgery consulted, not an acute abdomen. Constipation visible on KUB. Will use enema per surgery recommendations. Will follow lactates, exam.
2) Elevated lactate-- suggestive of ischemia. Pt with necrotic toe. This could be a possible other source of ischemia.
3) necrotic toe-- will consult vascular surgery regarding would care.
4) PAN -- marked systemic inflammation and constitutional sx's persist; Will continue Cytoxan, Solu-Medrol x 1 day, then prednisone 100 mg qd. Risedronate Q week for bone protection.
4) Anemia-- recent guaiac negative. Will obtain peripheral smear, retic count, B 12, folate, ferritin, TIBC. Secondary to chronic dz vs. renal insufficiency, vs loss.
5) will obtain foot x-ray, look for osteomyelitis in light of elevated ESR. Blood cx x 2.
6) Skin lesions-- will consult derm to see if they feel consistent with vasculitis. However, in light of pt poor healing, do not desire biopsy at this time.
7) Malabsorption-- study showed 11.9 g fat excreted over 24 hours, with 2-7 normal. Unsure of etiology-- bacterial overgrowth, secondary to dysmotility? Will consult GI for their input.
8) Pt is full code.

TOP

 

 

Operative Report8-18-03


PREOPERATIVE DIAGNOSIS:       Perforated abdominal viscus.
POSTOPERATIVE DIAGNOSIS:      Perforated small bowel.

OPERATION PERFORMED:      Segmental resection of small bowel with
               †††††††††† primary anastomosis.

ANESTHESIA:          †††† General endotracheal.

OPERATIVE DETAIL AND FINDINGS: The patient is a 47-year-old gentleman with polyarteritis nodosa whom we were consulted on this morning for abdominal pain and free air. He has been undergoing a steroid pulse for flare-up of his vasculitis and this complication has happened after a couple of days in the hospital.

After getting informed consent he was brought to the Operating Room where he underwent general endotracheal anesthesia. A Foley catheter was placed. Central line was placed in the right internal jugular vein and our resuscitation was continued with a central line as opposed to the peripheral line which was running more slowly. A left femoral arterial line was placed by anesthesia as he had no radial artery pulses that were palpable. He was then finally placed supine and prepped and draped in the usual manner. He had had a previous midline incision from a small bowel resection from a couple of years ago. It was unclear whether he had perforated or just strictured. In any event, his midline was opened. We gained access to his abdomen without any difficulty. There was really very little in the way of adhesions. There was some free air and there was some dirty dish brown-colored free peritoneal fluid with some odor to it in the abdominal cavity.

After getting the omentum off of his midline and freeing up a couple of colon that were stuck to some small bowel, we began to run his small bowel. From his ligament of Treitz it was about 8 inches down to an old jejunostomy feeding tube site. This was not obstructed. Then between the jejunostomy feeding tube site and the ileocecal valve there were two stapled side-to-side function end-to-end anastomoses indicating prior resections and there were four bowel perforations. There were two perforations such that it appeared that we could just resect two small segmental resections. The most distal one in the ileum amounted to about 8 inches of intestine and the more proximal one in the jejunum would require the removal of about 18 inches of intestine.

The intervening bowel between the two perforations was very mottled and hemorrhagic and it looked very compromised. The area around the punctate perforations was very mottled as well and it did not appear that it was a very safe thing just to oversew them. So we fired the GIA stapler across the bowel above and below the perforation in the areas of good bowel and we resected the mesentery in between 6-inch clamps and tied the stumps with 3-0 silk ties. We then did a functional end-to-end anastomosis with the GIA stapler and the TA-60 stapler. There were good staple line crossings and the bowel did not look compromised in the area that was reanastomosed.

We closed the mesenteric defects with running 3-0 Vicryl. At the end we ran the bowel again and there were not any other areas of compromise or perforation. We had resected about 24-inches of bowel and she had about 48 inches of bowel left in measuring it with an 18-inch free silk tie and measuring it across the antimesenteric border of the bowel and his ileocecal valve was intact. The stomach looked fine. Duodenum looked fine. Pancreas, liver and colon looked fine. His transverse colon was a little thin and dilated. The rectum looked fine.

We washed the abdomen out with about 6 liters of warm saline and aspirated all of the fluid. The feeding tube was then exchanged for a 12-French red rubber catheter. This feeding tube had been placed two years ago. It had never been used. The plastic was brown and discolored and partially filled with concretions, so it was simply removed in the Operating Room and then a new red rubber catheter placed in there and secured with a 2-0 silk stitch. The red rubber catheter was placed downstream of the insertion point. The original catheter had worked its way upstream.

The abdomen was then closed with running 1-0 Surgipro. The subcutaneous space was irrigated and the skin was closed with staples. He tolerated the procedure reasonably well. With the 4 liters of crystalloid he received during the two-hour operation his heart rate came down and his blood pressure stabilized and he made about 400 cc of urine. The blood loss was about 100 cc. He also received the beginning of what was going to be a 2-unit packed cell infusion for a HCT of about 27 at the beginning of the procedure. All sponge counts, needle counts and instrument counts were correct. He was taken to the ICU intubated following the procedure, having tolerated it reasonably well.

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Clinical Laboratory Report

 

 

Collected Date  

Resulted Date  

Order Description  

Status  

Accession# 

Provider  

08/16/02

 

PT/INTERNAT. NORMALIZED RATIO

Final

 

 

Name

Result/Unit

 

Ref Interval

Status

PROTHROMBIN TIME

28.5 sec

H

12.0-15.5

 

INTERNATIONAL NORMALIZED RATIO

2.7 ratio

 

 

 

 

Comments:
REFERENCE INTERVAL: International Normalized Ratio (INR)
INR values should only be used when evaluating patients
on oral anticoagulant therapy.
 
INR 2.0 - 3.0 : Prophylaxis of venous thromboembolism,
                treatment of venous thrombosis (following
                heparin therapy), prevention of systemic
                embolism (atrial fibrillation, valvular
                heart disease, bioprosthetic heart valves,
                acute myocardial infarction).
 
INR 2.5 - 3.5 : Mechanical prosthetic heart valves,
                recurrent systemic embolism.

 

08/16/03

 

LACTIC ACID

Final

 

 

 

 

Name

Result/Unit

 

Ref Interval

Status

LACTIC ACID

2.9 mmol/L

H

0.5-2.2

 

 

08/16/03

 

HEPATIC FUNCTION PANEL

Final

 

 

 

 

Name

Result/Unit

 

Ref Interval

Status

ALBUMIN

2.7 g/dL

L

3.5-4.6

 

BILIRUBIN, TOTAL

0.3 mg/dL

 

0.2-1.3

 

ALKALINE PHOSPHATASE

59 U/L

 

38-126

 

ASPARTATE AMINOTRANSFERASE

12 U/L

L

15-59

 

ALANINE AMINOTRANSFERASE

15 U/L

 

13-72

 

BILIRUBIN, DIRECT

0.3 mg/dL

 

0.0-0.4

 

TOTAL PROTEIN

5.4 g/dL

L

6.3-8.2

 

 

08/16/03

 

CBC WITH PLTS AND MANUAL DIFF

Final

 

 

 

 

Name

Result/Unit

 

Ref Interval

Status

WHITE BLOOD CELL COUNT

4.15 K/uL

 

3.20-10.60

 

RED BLOOD CELL COUNT

2.20 M/uL

L

4.69-6.07

 

HEMOGLOBIN

7.9 g/dL

L

14.6-17.8

 

HEMATOCRIT

22.5 %

L

40.8-51.9

 

MEAN CORPUSCULAR VOLUME

102.4 fL

H

77.8-94.0

 

MEAN CORPUSCULAR HEMOGLOBIN

36.1 pg

H

26.5-32.6

 

MEAN CORPUSCULAR HGB CONC

35.2 g/dL

 

32.7-36.9

 

RED CELL DISTRIBUTION WIDTH

18.0 %

H

10.8-14.1

 

PLATELETS

379 K/uL

 

177-406

 

MEAN PLATELET VOLUME

8.1 fL

 

5.9-9.8

 

POLYMORPHONUCLEAR

72 %

 

44-76

 

BAND

25 %

H

0-5

 

LYMPHOCYTE

2 %

L

15-43

 

EOSINOPHIL

1 %

 

0-6

 

PLATELET ESTIMATE

ADEQUATE

 

NORMAL

 

ANISOCYTOSIS

2+

A

 

 

POIKILOCYTOSIS

1+

A

 

 

MACROCYTOSIS

1+

A

 

 

POLYCHROMASIA

1+

A

 

 

 

08/16/03

 

SMEAR INTERPRETATION

Final

 

 

 

 

Name

Result/Unit

 

Ref Interval

Status

SMEAR INTERPRETATION

SEE NOTE

 

 

Final

 

Comments:
DIFFERENTIAL:  Segs 85, bands 13, monos 1, lymphs 1.
MORPHOLOGY:  Erythrocytes are normochromic and macrocytic and exhibit moderate
anisopoikilocytosis.  Macrocytes and burr cells are readily identified.
Myeloid forms comprise the predominant leukocyte population and demonstrate a
shift to immaturity, with increased numbers of bands identified.  Lymphocytes
are markedly reduced in number.  Platelets are adequate in number and
unremarkable in morphology.
PERIPHERAL BLOOD:
    - NORMOCHROMIC, MACROCYTIC ANEMIA WITH MODERATE ANISOPOIKILOCYTOSIS.
    - RELATIVE NEUTROPHILIA WITH SHIFT TO IMMATURITY IN MYELOID SERIES.
    - ABSOLUTE LYMPHOPENIA.

 

08/16/03

 

BASIC METABOLIC PANEL

Final

 

 

 

 

Name

Result/Unit

 

Ref Interval

Status

SODIUM

133 mmol/L

L

136-144

 

POTASSIUM

3.3 mmol/L

 

3.3-5.0

 

CHLORIDE

95 mmol/L

L

98-107

 

CARBON DIOXIDE

28 mmol/L

 

22-29

 

UREA NITROGEN

21 mg/dL

 

9-22

 

CREATININE, SERUM - mg/dL

1.5 mg/dL

 

0.8-1.5

 

GLUCOSE

117 mg/dL

 

64-128

 

ANION GAP

10 mmol/L

 

8-14

 

CALCIUM, SERUM OR PLASMA

8.2 mg/dL

L

8.4-10.2

 

 

TOP


Clinical Laboratory Report

Collected Date  

Resulted Date  

Order Description  

Status  

Accession# 

Provider  

Source

08/21/03

 

ABG with Electrolytes, Lactate and Gluc, Arterial, Delivered

Name

Result/Unit

 

Ref Interval

Status

FiO2

40 %

 

 

 

pH

7.493

H

7.35-7.45

 

PaCO2

28.4 mmHg

L

35-39

 

PaO2

69.1 mmHg

 

61-82

 

COHb

0.6 %

 

0.1-2

 

MethHb

0.7 %

 

0.1-2

 

tHb

9.2 gm%

L

13-19

 

O2 Content

12.1 vol%

L

17-24

 

Pb

632 mmHg

 

 

 

A-aO2

131 mmHg

 

 

 

Na+

138 mmol/L

 

136-144

 

K+

3.9 mmol/L

 

3.3-5

 

Ca++

1.04 mmol/L

L

1.11-1.3

 

HCO3

21.6 mEq/L

 

19-25

 

BE

-0.7 mEq/L

 

-2.5-2.5

 

O2Hb

92.2 %

 

92-99

 

Hct

28.6 g/dL

 

 

 

Glucose

121 mg/dL

H

65-110

 

Lactate

2.2 mmol/L

H

0.7-2.1

 

Temp

37.9 C

 

 

 

Allen`s Test

N

 

 

 

PaO2*

73.3 mmHg

 

61-82

 

08/21/03

 

CBC with PLATELET COUNT

Final

 

 

 

Name

Result/Unit

 

Ref Interval

Status

WHITE BLOOD CELL COUNT

7.48 K/uL

 

3.20-10.60

 

RED BLOOD CELL COUNT

2.89 M/uL

L

4.69-6.07

 

HEMOGLOBIN

9.2 g/dL

L

14.6-17.8

 

HEMATOCRIT

27.2 %

L

40.8-51.9

 

MEAN CORPUSCULAR VOLUME

94.1 fL

H

77.8-94.0

 

MEAN CORPUSCULAR HEMOGLOBIN

31.8 pg

 

26.5-32.6

 

MEAN CORPUSCULAR HGB CONC

33.8 g/dL

 

32.7-36.9

 

RED CELL DISTRIBUTION WIDTH

18.5 %

H

10.8-14.1

 

PLATELETS

24 K/uL

L

177-406

 

MEAN PLATELET VOLUME

7.8 fL

 

5.9-9.8

 

08/21/03

 

BASIC METABOLIC PANEL

Final

 

 

 

Name

Result/Unit

 

Ref Interval

Status

SODIUM

137 mmol/L

 

136-144

 

POTASSIUM

4.1 mmol/L

 

3.3-5.0

 

CHLORIDE

108 mmol/L

H

98-107

 

CARBON DIOXIDE

25 mmol/L

 

22-29

 

UREA NITROGEN

37 mg/dL

H

9-22

 

CREATININE, SERUM - mg/dL

2.4 mg/dL

H

0.8-1.5

 

GLUCOSE

129 mg/dL

H

64-128

 

ANION GAP

4 mmol/L

L

8-14

 

CALCIUM, SERUM OR PLASMA

6.3 mg/dL

L

8.4-10.2

 

08/20/03

 

PROTHROMBIN TIME

Final

 

 

 

Name

Result/Unit

 

Ref Interval

Status

PROTHROMBIN TIME

28.3 sec

H

12.0-15.5

 

08/20/03

 

PARTIAL THROMBOPLASTIN TIME

Final

 

 

 

Name

Result/Unit

 

Ref Interval

Status

PARTIAL THROMBOPLASTIN TIME

66 sec

H

26-37

 

TOP


Microbiology Report

Collected Date  

Resulted Date  

Order Description  

Status  

08/20/03

 

RESPIRATORY CULTURE, SPUTUM

Final

Name

Result

GRAM STAIN

NO ORGANISMS SEEN

GRAM STAIN

NO PMNS SEEN

FINAL REPORT

1+ MOULD

FINAL REPORT

NO OTHER FLORA ISOLATED

 

08/20/03

 

BLOOD CULTURE, BOTTLE SYSTEM, BLOOD, CENTRAL LINE

Final

Name

Result

FINAL REPORT

NO GROWTH

 

08/20/03

 

BLOOD CULTURE, BOTTLE SYSTEM, BLOOD, L WRIST

Final

Name

Result

FINAL REPORT

NO GROWTH

 

08/20/03

 

URINE CULTURE, URINE

Final

Name

Result

FINAL REPORT

NO GROWTH

 

08/16/03

 

BLOOD CULTURE, BOTTLE SYSTEM, BLOOD, "RIGHT ANTECUBITAL"

Final

Name

Result

FINAL REPORT

NO GROWTH

 

08/16/03

 

BLOOD CULTURE, BOTTLE SYSTEM, BLOOD, "LEFT HAND"

Final

Name

Result

FINAL REPORT

NO GROWTH

TOP



SEDIMENTATION RATE, WESTERGREN Trend

Date

Result/Unit

H/L

Ref Interval

Comments

03/21/03 04:25 PM 

23 mm/hr 

H

0-10  

 

02/14/03 05:28 PM 

14 mm/hr 

H

0-10  

 

01/17/03 04:00 PM 

10 mm/hr 

 

0-10  

 

12/07/02 02:10 PM 

50 mm/hr 

H

0-10  

 

TOP

 

 

 

Radiology Report

Exam Date

Study Description

Status

Ordering Provider

 

 

08/21/2003

CHEST XRAY 1V

Final

 

 

 

HISTORY : Vasculitis, abdominal pain

COMPARISON : 8/20/03, 8/19/03

FINDINGS : AP view of the chest is obtained. This is a
technically limited study with exclusion of the bases.
CHEST TUBES AND CATHETERS: There is a right IJ catheter with tip
in the SVC. The endotracheal tube is 6 cm above the carina. The
nasogastric tube extends below the margins of the study.
LUNG INFLATION: Lung inflation is normal.
PULMONARY PARENCHYMA: There is increased opacity of the right
hemithorax and the left lower lobe. There is increased left
retrocardiac opacity, consistent with effusion, atelectasis or
consolidation. Kerley B lines are present.
PLEURAL SPACE: There is increased bilateral pleural effusion.
There is no pleural thickening or pneumothorax.
CARDIAC AND MEDIASTINAL CONTOURS : The cardiac and mediastinal
silhouettes are unchanged.
PULMONARY VESSELS: Pulmonary vasculature is indistinct.
CHEST WALL AND SOFT TISSUE: There are no osseous or soft tissue
lesions.

IMPRESSION: 1. INCREASED PULMONARY EDEMA. 2. INCREASED
BILATERAL PLEURAL EFFUSION. 3. TECHNICALLY LIMITED STUDY WITH
EXCLUSION OF THE LEFT BASE.

 

08/20/2003

CHEST XRAY 1V

Final

 

 

 

HISTORY: Atelectasis, vasculitis, abdominal pain.

FINDINGS: Comparison with 1990s- 2002 at 0547 hours.

The cardiomediastinal silhouette is unchanged. There is
increasing vascular enlargement and indistinctness with interval
development of Kerley B lines and increasing diffuse hazy opacity
throughout the lungs bilaterally. Left retrocardiac consolidative
opacity is unchanged. No other change in the pulmonary
parenchymal or vascular markings seen. The endotracheal tube, NG
tube, and right internal jugular central venous sheath are
unchanged. No other definite interval changes are seen.

IMPRESSION: Increasing changes of pulmonary edema as described.
Increased diffuse density has configuration suggesting posterior
layering pleural effusions bilaterally.
Left basilar consolidation may represent atelectasis, aspiration,
or infiltrate. Correlation with clinical findings recommended.

 

08/19/2003

CHEST XRAY 1V

Final

 

 

 

History: Vasculitis.

Findings: Comparison study is dated 8/18/02. The tubes and lines
are unchanged in appearance. Increasing opacity within the left
lower lobe is seen resulting in obscuration of the left
hemidiaphragm. No pleural effusions are identified. There is no
evidence of pulmonary edema. The osseous structures are stable in
appearance.

Impression: New ill-defined opacity seen within the left lower
lobe with obscuration of the left hemidiaphragm. Differential
considerations include atelectasis versus pneumonia.

 

 

08/18/2003

CHEST XRAY 1V

Final

 

 

 

HISTORY: Suspected free air under the diaphragm

FINDINGS
Lungs are clear with no evidence of consolidation or pulmonary
edema.
Normal size and configuration of the cardiomediastinal silhouette.
The costophrenic recesses are clear bilaterally with no evidence
of pleural effusions or pneumothorax.
There is evidence of free air under the right hemidiaphragm.

IMPRESSION: NO EVIDENCE OF ACUTE CARDIOPULMONARY PROCESS.
FREE AIR UNDER THE RIGHT HEMIDIAPHRAGM.

 

08/18/2003

ABDOMEN 1 VIEW

Final

 

 

 

PROCEDURE: Abdomen single view

REASON FOR EXAM: Abdominal pain

FINDINGS: Free intra-abdominal air seen suggesting bowel
perforation. Large amount of fecal material seen in the colon.
No abnormal calcifications seen or evidence of organomegaly. Left
sided tube seen ending in the abdominal cavity. Status post
cholecystectomy with surgical clips in the right hypochondrium.


IMPRESSION: Free intraperitoneal air suggesting bowel
perforation.

 

 

08/16/2003

FOOT 2 VIEW

Final

 

 

 

LEFT FOOT: 08/16/2002.

HISTORY: Evaluate for osteomyelitis.

FINDINGS: There is a bipartite lateral sesamoid. This is of no
clinical significance. There are no areas of rarefaction to
suggest osteomyelitis.

IMPRESSION: NO EVIDENCE OF RAREFACTION TO SUGGEST OSTEOMYELITIS.

 

TOP

 

Old CXR for comparison (12-7-02):

†† †††

TOP

 

Death Summary 08/21/03

 

Adm Date:    08/16/03
Disc Date:††
08/21/03

ADMISSION DIAGNOSIS:
Abdominal pain and polyarteritis nodosa.

OTHER DIAGNOSES:
1. Hypertension.
2. Raynaud's.
3. Status post small-bowel resection and jejunostomy tube placement.
4. Renal insufficiency.
5. Gangrene of left first and second toes.

PROCEDURE:
SURGICAL: Small-bowel resection with primary anastomosis on
08/18/2002.

HISTORY: Patient was a 46-year-old male with a diagnosis of polyarteritis nodosa diagnosed in December 2001 who had been on treatment regimens of steroids and Cytoxan with persistent and active inflammation. He had had necrotic toes which required amputation; malabsorption issues and positive fecal fat studies. He was seen by Rheumatology who noted the persistent inflammation and new vasculitic appearing leg ulcers. He had persistent weight loss due to malabsorption. High dose Solu-Medrol was given for two days with increases of his prednisone to 100 mg q.d. On the second day of Solu-Medrol infusion he had severe abdominal pain.


PAST MEDICAL HISTORY: As above. In addition, he had ischemic bowel with resection of small bowel back in December 2002 and then dry gangrene of great and second toes, hypertension, J-tube placement, and a cholecystectomy.

PHYSICAL EXAMINATION: VITAL SIGNS: He was febrile, pulse 93, blood pressure 140/82.

ABDOMEN: Soft, nondistended, with bilateral lower abdominal tenderness.

LABORATORY DATA: Total white count of 5.1 with 70% polys, bands 25, 2% lymphs, hematocrit at 25, lactate of 5.9, and an INR of 2.7.

Abdominal films at that time showed a large amount of colonic fecal material with no evidence of intestinal obstruction or free intra-abdominal air.

HOSPITAL COURSE: The initial assessment was abdominal pain with a further plan to obtain a Surgery consult and elevated lactate which was felt to be due to the patient's necrotic toe. Polyarteritis nodosa treated with Cytoxan, Solu-Medrol, and prednisone. Anemia was being worked up.

Late on the first hospital day, Surgery consult was obtained which at that time the patient had no evidence of an acute abdomen and the initial assessment was thought to be due to constipation/dehydration. However, early on the third hospital day, the Surgery Team was called to see the patient in regards to increasing abdominal distention and free air on the chest x-ray and the patient had a lactate of 4.6 at that time and was taken to the operating room emergently for an exploratory laparotomy. For details, please see operative report, but during the exploratory laparotomy they found two perforations repaired by two small segmental resections with primary anastomosis.

Postoperatively the patient was not doing well and by the second postoperative day he became increasingly unstable with increasing tachypnea and tachycardia with fevers to 40 degrees Celsius. His abdomen was increased in distention and his lactate was starting to rise. At this time, concern regarding an intra-abdominal process with perforation or anastomotic leak was discussed with the family and a grave prognosis was shared with them who at this time wished to only continue supportive measures and did not wish to continue any aggressive care. The patient was made DNR with no further operations. He was maintained on supportive care with IV antibiotics and fluids and pain control.

The patient was managed with palliative care until
08/21/2002 where he continued to deteriorate and the family elected to withdraw support and the patient did expire one hour later.

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autopsy Pathology Report

AU CASE INFORMATION

SEX: M AGE: 46
DATE OF AUTOPSY:
08/23/03


AUTOPSY CAUSE OF DEATH: Pneumonia
DUE TO: Sepsis
DUE TO: Perforated bowel
DUE TO: Polyarteritis nodosa.
------------------------

AU CASE SUMMARY

CLINICAL HISTORY: The patient was a 46-year-old male, veteran of the Gulf war. His past medical history was significant for hypertension, mononeuritis multiplex, Raynaud's phenomenon, chronic renal insufficiency, macrocytic anemia, and polyarteritis nodosa with complications including ischemic bowel (status post two small bowel resections and jejunostomy tube placement) dry gangrenous left big toe and left second toe, renal insufficiency and livedo reticularis. He was also a heterozygote for factor V Leiden. He has a sister with history of Raynaud's syndrome. The patient had been on steroids and Cytoxan due to concerns of malabsorption and persistent evidence of inflammation (ESR 82). He was to receive Solu-Medrol for two days and prednisone, 100 mg qd. The patient was receiving his second high dose of Solu-Medrol when he developed abdominal pain. The patient was admitted. Abdominal x-rays at that time demonstrated a large amount of stool without free air. No acute surgical intervention was taken and the patient was given IV fluids, an enema and magnesium citrate without results. Labs on admission were: Sodium 133, potassium 3.3, chloride 95, C02 28, urea nitrogen 21, serum creatinine 1.5, glucose 117; the white blood cell count was 5.1, hematocrit 25.3, platelets 379; AST 12, ALT 15, alkaline phosphatase 59, albumin 2.7, total bilirubin 0.3, PT 28.5, INR 2.7, lactate 5.9, lipase 41, amylase 56. The patient's stool was guaiac negative. During the next 24 hours the radiology report was revised to read "questionable sub-diaphragmatic lucency on the left which may represent free air". The patient was taken to surgery, where four perforations were noted between the jejunostomy site and the ileocecal valve. Two sections of small intestine were removed, the proximal portion measuring 18 inches and the distal portion measuring 8 inches. An end-to-end anastomosis was performed. The patient was intubated and sedated. He did relatively well the first 12 hours status post surgery. However, his pH continued to drop, he was dependent on the ventilator, and became hemodynamically unstable. Chest x-ray on 8-20-02 suggested posterior pleural effusions bilaterally. Labs on 8-21-02 were as follows: WBC 7.5, hematocrit 27.2, platelets 24, potassium 4.1, urea nitrogen 37, serum creatinine 2.4, ABG's 7.49\28.4\73.3\21.6. The family decided not to continue aggressive care and support was withdrawn. The patient expired on August 21st, 2002, 1540.


At autopsy, numerous skin lesions were present (ulcerations and eschar). The left great toe and left second toe were necrotic. Several areas of necrosis were found in the stomach, duodenum and colon. There was evidence of peritonitis, gastrohepatic adhesions, and 100 cc of ascites (serous). Multiple infarcts were seen in the kidneys, adrenals, and testicles. Microscopically, scarring and recanalization of medium-sized vessels was noted in the mesentery, stomach, spleen, liver, and kidneys. The lungs demonstrated mild bronchopneumonia and early diffuse alveolar damage. A 675 cc right serous pleural effusion, and 1000 cc left serous pleural effusions were present. The bone marrow as hypocellular (40%), consistent with the patient's use of Cytoxan. Overall, the findings are suggestive of classic polyarteritis nodosa. Typical features of this disease include livedo reticularis, necrotic lesions, infarcts of the digits, and mononeuritis multiplex. Involvement of the medium-sized arteries in the skin, gastrointestinal tract, and kidneys, is also consistent with PAN. ANCA tests are often negative.

 

Immediate cause of death was pneumonia, due to sepsis after perforation of the small bowel. The small bowel perforations were likely a complication from PAN. Being heterozygous for Factor V Leiden also increased this patient's risk for venous thrombosis.

------------------------

 

AU FINAL DIAGNOSIS

CLINICAL DIAGNOSES:
1. Heterozygous for factor V Leiden.
2. Polyarteritis nodosa
†† A) Small bowel ischemia status post two small bowel resections
†† B) Dry gangrenous left great toe and left second toe.
†† C) Renal insufficiency.
†† D) Livedo reticularis.
3. Macrocytic anemia.
4. Hypertension.
5. Raynaud's syndrome.
6. Mononeuritis multiplex.


FINAL ANATOMIC DIAGNOSES:
I. Early diffuse alveolar damage and bronchopneumonia.
†† A) Right pleural serous effusion 675 cc.
†† B) Left pleural serous effusion 1,000 cc.
II. Serous pericardial effusion 30 cc.
III. Polyarteritis nodosa (12/01) (SP-01-12921).
††† A) Areas of necrosis in colon, duodenum and stomach with gastrohepatic
†††††† adhesions.
†††††† 1) Peritonitis.
†††††† 2) Ascites 100 cc serous fluid.
†††††† 3) Status post small bowel excision 96.5 cm (SP-02-8250).
†††††† 4) Jejunostomy site patent.
†††††† 5) Midline incision with staples clean and healing.
†† B) Skin lesions.
†††††† 1) Ulcer - left lateral malleolus.
†††††† 2) Black eschar - left shoulder.
†††††† 3) Eschar left elbow.
†††††† 4) Eschar/ulcer right Achilles 2.4 x 2.7 cm.
†††††† 5) Ulcer right heel 6.2 x 5.7 cm.
†††††† 6) Necrotic great left toe and left 2nd toe.
†† C) Multiple old infarcts of kidneys.
†† D) Focal testicular infarcts.
IV. Incidental findings:
†† A) Surgically absent gallbladder.
†† B) Scrotal edema.
†† C) Diffuse hair loss.
†† D) Mild scoliosis.
V. Neuropathology report to follow.
------------------------

 

AU GROSS DESCRIPTION

EXTERNAL EXAMINATION: A duly executed permit for autopsy is received from the wife. The body length is 185 cm crown-to-heel and 79 cm crown-to-rump. The body is estimated to weigh 77.3 kg. The body is that of a normally developed Caucasian male who appears much older than the stated age of 46 years. His body habitus is cachectic. The head circumference is 56 cm, the head is normal in size and the shape is symmetric. The hair distribution is normal and the texture is fine. The scalp hair is light brown to gray and medium length (7 cm) and shows baldness over the frontal and vertex area. The face is not remarkable. The eyes are normal and blue in color. The right pupil measures 4.0 mm and the left pupil measures 5.0 mm. The ears are normal. The nose, mouth and neck are normal. There is 4+ dependent livor of the posterior and 0 rigor mortis. A 3.8 x 1.2 cm scar is present over the left shoulder. A 1.2 cm area of ulceration is present on the mid-back, and a 3.4 cm ulceration is present on the right buttocks. The right medial malleolus has a 2.4 x 2.7 ulcer. The right Achilles has a 6.2 x 5.7 cm ulcer and the right arch of the foot has a 1.0 cm ulcer. A 7.8 cm scar is present on the anterior right leg, and a 1.0 cm scar is present on the medial aspect of the left knee. The lower extremity calf muscles are thin and the legs are hairless. A 24 cm abdominal incision is present, held together with staples. An old jejunostomy site measuring 3.0 cm is present in the left lower quadrant. Intravenous access lines are found on both forearms bilaterally. The chest circumference is 89 cm and the chest is symmetric. The breasts are normal and the chest hair is scanty. The abdominal circumference is 78 cm and the abdomen is flat. The back shows minimal scoliosis with a major curve to the right. The external genitalia are normal for male sex. The penis is circumcised and the scrotum is edematous. The extremities show no clubbing. However, the left great toe and left second toe show dry gangrene.
CENTRAL NERVOUS SYSTEM: A bitemporal incision is performed and the calvarium is removed. The scalp is normal. The skull is of average thickness. The middle ears are not examined. The dura is normal. The meninges are normal. The cerebral vessels show no atherosclerosis. The brain weighs 1,410 grams. The brain and spinal cord are saved for further neuropathologic examination.
THORACIC CAVITY: A "Y" incision is made. The subcutaneous fat measures 0.7 cm at the level of the nipples. Organ situs in the thorax is normal. The pleural surfaces are smooth and glistening. The pleural cavities contain 675 cc on the right and 1,000 cc on the left of serous fluid. A pneumothorax is not found. The mediastinum is without lesions.
ABDOMINAL CAVITY: A midline incision is made. The fat measures 1.2 cm at the level of the liver. Organ situs in the abdomen is normal. The diaphragmatic dome heights are at the level of the sixth rib on the right and sixth rib on the left. The liver is 2.5 cm below the right costal margin at the midclavicular line. The peritoneal surfaces show fibrous adhesions and purulent exudate. The peritoneal cavities contain 100 cc of serous fluid. The retroperitoneum is without lesions. The stomach contains dark brown fluid. There appears to be an area of retrogastric hemorrhage.
CARDIOVASCULAR SYSTEM: The heart weighs 352 grams. The pericardial cavity contains 30 cc of serous fluid. The epicardium is smooth and glistening and the epicardial fat is of the usual amount. The heart chambers are not dilated. The right ventricular thickness is 0.5 cm and the length is 8.4 cm. The left ventricular thickness is 1.5 cm and the length is 8.1 cm. The atrial appendages are free of thrombi. The foramen ovale is closed. The myocardium is firm and brown, with no fibrosis. The endocardium is thin and translucent. The trabeculae carneae and papillary muscles are normal. The chordae tendineae
are normal. The heart valves are thin and pliable. The heart valve ring circumferences are: 13.0 cm tricuspid; 7.0 cm pulmonic; 10.2 cm mitral; 6.5 cm aortic. The coronary arteries show right dominance with minimal atherosclerosis and no narrowing of all branches. Thrombosis of no vessels is found. The aorta is elastic and shows no atherosclerosis. The major branches are all patent. The vena cava are patent.
RESPIRATORY TRACT: The pharynx, larynx, trachea and mainstem bronchi are without lesions. The right lung weighs 870 grams and the left lung weighs 700 grams. The pleural surfaces are smooth. The lungs are inflated with formalin prior to sectioning. The pulmonary parenchyma shows posterior congestion. On sectioning, the parenchyma shows areas of patchy consolidation in the upper lobes. Tumor masses and granulomas are not seen. The cut surfaces of the lungs are pink and exude no fluid. Anthracotic pigmentation is not marked. The bronchi are normal. The pulmonary arteries do not have premortem thromboemboli. The pulmonary arteries have no atherosclerosis. The pulmonary veins are clear.
GASTROINTESTINAL TRACT: The tongue is normal. The submandibular salivary glands are not examined. The esophagus is without lesions. The stomach contains dark brown fluid. The gastric mucosa shows several areas of erosion. The esophagus is without lesions and the stomach contains dark brown fluid. The gastric mucosa shows several areas of erosion. The rugal pattern is normal. The pylorus is patent and the duodenum shows several areas of necrosis. The remaining small intestine (approximately 4 feet) is patent at the area of the old jejunostomy site. The mucosa is velvety and the folds are normal. The appendix is normal. The large intestine is normal. The mucosa is velvety and the mucosal folds are normal. The bowel contents consist of a moderate amount of soft green stool. The mesenteric arteries and veins appear grossly normal.
PANCREAS: The pancreas measures 15.2 x 2.5 x 1.6 cm and is the usual size, firm, with normal architecture. Fat necrosis is not present. The pancreatic duct is patent with no stones and enters the duodenum at the ampulla of Vater.
HEPATOBILIARY SYSTEM: The liver weighs 2,050 grams. The liver capsule is smooth and glistening. The liver edge is sharp. The hepatic parenchyma is firm and brown. Cirrhosis is not present and a lobular pattern is not visible. Tumor masses are not seen. The portal vein, hepatic artery and hepatic veins are patent. The gallbladder is absent. The cystic duct, extrahepatic ducts,and intrahepatic ducts are patent. The ampulla of Vater is normal.

SPLEEN AND LYMPHATIC SYSTEM: The spleen weighs 200 grams. The splenic capsule is smooth and translucent with no lesions. The splenic parenchyma is dark red and soft. The follicular and trabecular pattern is not visible. There are no accessory spleens found. The splenic artery and splenic vein are patent.
URINARY SYSTEM: The right kidney weighs 82 grams and the left kidney weighs 90 grams. The capsules strip with ease. The cortical surfaces of the kidneys are pale red, smooth, and nodular, with many V-shaped scars. The cut surfaces are pale red. The right cortical thickness ranges from 0.3 cm to 0.9 cm. The left cortical thickness ranges from 0.5 cm to 1.0 cm. The corticomedullary demarcations are good. The medullae are red. There are no cysts present. The pyramids are normal. The calyces and pelves are normal. The uterus are normal and enter the bladder at the trigone. The bladder is the usual size with a thin wall and smooth mucosa throughout. A catheter is not present. The bladder
contains a small amount of yellow urine and no calculi. The urethra is patent.
The renal arteries show no atherosclerosis. The renal veins are clear.
MALE GENITAL SYSTEM: The prostate is normal in size and firm with the usual appearance. The seminal vesicles are normal. The testicles are normal. On sectioning they are pale brown and soft in consistency. The tubules string poorly. The epididymides are normal.
ENDOCRINE GLANDS: The pituitary is the usual size, shape, and color. The thyroid weighs 28.1 grams and is the usual size. The thyroid has the usual shape, color and consistency. On sectioning the parenchyma is red-brown and firm with no nodules. No parathyroid glands are found. The right adrenal gland weighs 8.5 grams and the left adrenal gland weighs 8.3 grams. The adrenals are normal in size with the usual shape, color, and consistency. Their cortices have the usual appearance. The medullae are normal.
MUSCULOSKELETAL SYSTEM: The body and extremities are symmetric with no
malformations. Skeletal muscles are red-brown. There is evidence for muscle wasting in the lowerextremities bilaterally. Bone deformities are not present. Cardiopulmonary resuscitation was not performed. The joints are not examined. The vertebral bone marrow is red and the vertebral bone is normal in consistency.
CASSETTE SUBMISSION:
A - Bone marrow (rib).
B - Left and right adrenal.
C - Pituitary.
D - Septum, left anterior descending coronary artery, and left ventricle.
E - Right ventricle and right circumflex artery.
F - Base of first and second left toes.
G - Spleen with vessels.
H - Diaphragm.
I - Mesentery.
J - Stomach and pancreas.
K - Retrogastric hemorrhage.
L - Liver.
M - Lung - right upper lobe.
N - Lung - right middle lobe.
O - Lung - right lower lobe.
P - Bone.
Q - Lung - left upper lobe.
R - Lung - left lower lobe.
S - Thyroid.
T - Testes.
U - Right kidney.
V - Left kidney.
W - Bladder and prostate.
X - Colon - cecal area.
Y - Diaphragm
------------------------

 

AU MICROSCOPIC DESCRIPTION

Bone Marrow: Sections of bone marrow from the rib (cassette A) demonstrate
hypocellularity, estimated at 40%. All three cell lines are identified with a
myeloid to erythroid ratio of 3:1.
Mesentery: Sections of the mesentery (cassette I) demonstrate scarring and
recanalization of the medium sized arteries. The larger vessels demonstrate
no abnormalities. Elastin stain demonstrates intact elastic lamina.
Diaphragm: A section of diaphragm (cassette H and Y) demonstrates muscle loss
and acute inflammation.
Pancreas: A section of pancreas (cassette J) demonstrates no abnormalities.
Stomach: A section of stomach (cassette J) demonstrates areas of vascular
destruction. Sections of the posterior stomach (cassette K) show fat necrosis
and recanalized vessels. There is also acute inflammation. Elastin stain
demonstrates intact elastic lamina.
Spleen: Sections of the spleen (cassette G) demonstrate amorphous material
surrounding the lumens of medium to small sized vessels. The larger vessels
demonstrate no abnormalities. Trichrome stains show occlusion and fibrin
deposition in the walls of medium to small sized vessels. Congo Red stain is
negative for amyloid.
Liver: Sections of the liver (cassette L) demonstrate some bile stasis. There
is minimal steatosis and the medium sized arteries have thickened walls. Iron
stain is negative.
Lung: Sections of the lung (cassettes M, O, Q, R) demonstrate patchy
bronchopneumonia and early diffuse alveolar damage. Note: There is a floater
in cassette M.
Heart: Sections of the left anterior descending coronary artery (cassette D)
demonstrate a thickened wall with medial hypertrophy and fibrosis. The left
ventricle and septum demonstrate no abnormalities. The right ventricle
(cassette E) demonstrates no abnormalities. The right coronary artery
(cassette E) shows eccentric scarring and fibrosis. There is evidence of old
vascular disease and calcifications in several of the vessels.
Adrenals (cassette B): The adrenals show several nodules of hyperplasia in
the cortex and also demonstrate several areas of infarct.
Kidney: Sections of kidney (cassettes U and V) demonstrate thyroidization of
the kidney. There are vessels that have been completely occluded and
recanalized, and evidence of old scarring and infarcts. Some vessels are
suspicious for thrombotic disease. There is a loss of glomeruli. Elastin
stain shows damaged elastic lamina in several vessels.
Prostate: A section of prostate (cassette W) demonstrates no abnormalities.
Note: There is a floater in cassette W.
Bladder: A section of bladder (cassette W) demonstrates no abnormalities.
Colon (cecal area): Sections of the large intestine (cassette X) demonstrates
necrosis and peritonitis.
Testes: Sections of the testicle (cassette T) demonstrate infarcted areas of
the seminiferous tubules. There is no evidence of sperm production.
Pituitary: A section of the pituitary (cassette C) shows no abnormalities.
Thyroid: A section of thyroid (cassette S) demonstrates no abnormalities.
Base of first and second left toes: Sections of the base of the first and
second left toes (cassette F) demonstrate areas of ulceration and scarred
vessels. Elastin stain demonstrates one vessel with destroyed elastic
lamina. There is no evidence of active polyarteritis nodosa.
Bone: A section of bone demonstrates hypocellular marrow and osteopenic bone.
------------------------

 

TOP

 

 

Laboratory Normal Values:

 

ACTH††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 9 - 52 pg/mL

Alpha-fetoprotein††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 0 - 15 ng/mL

Alanine aminotransferase (ALT)††††††††††††††††††††††††††††††††††††††††††† 6 - 50 U/L

Albumin††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 3.5 - 4.6 g/dL

Alkaline phosphatase†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 45 - 150 U/L

Ammonia†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 7 - 27 micromol/L

Amylase, serum (adult)†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 30 - 110 U/L

Aspartate aminotransferase (AST)†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 15 - 50 U/L

Bilirubin, total†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 0 - 1.5 mg/dL

Bilirubin, direct†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 0 - 0.3 mg/dL

Calcium††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 8.8 - 11.0 mg/dL

Carbon dioxide†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 20 - 29 mmol/L

Catecholamines, urine free††††††††††††††††††††††††††††††††††

††††††††††††††††††† Epinephrine††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 0 - 25 microgm/day

††††††††††††††††††† Norepinephrine††††††††††††††††††††††††††††††††††††††††††††††††††††† 0 - 100 microgm/day

Chloride†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 101 - 111 mmol/L

Cholesterol, total†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 100 - 200 mg/dL

Cholesterol, HDL†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 0 - 35 mg/dL

Cortisol †††† (8 am)†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 6 - 23 microgm/dL

††††††††††††††††††† (8 pm)††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 0 - 9 microgm/dL

Creatine kinase†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 20 - 200 U/L

Creatinine††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 0.8 - 1.4 mg/dL

Erythrocyte sedimentation rate†††††††††††††††††††††††††††††††††††††††††††††† 0 - 20 mm/Hr

Estradiol, female†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† <73 pg/mL (postmenopausal)†††††††††††††††††††††††††††††

††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 30 - 400 pg/mL (normal hormonal cycle)

Ferritin†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 7 - 340 ng/mL (male)

††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 7 - 75 ng/mL (female)

Gastrin†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 0 - 100 pg/mL

Glucose†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 64 - 128 mg/dL

HCG, serum, quantitative

††††††††††††††††††† Male††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 0 - 5 IU/L

††††††††††††††††††† Female†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 2 - 8 IU/L

Homocysteine, plasma††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 4 - 12 micromol/L

Homovanillic acid (HVA), urine††††††††††††††††††††††††††††††††††††††††††††† 0 - 15 mg/day

Iron, serum†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††

††††††††††††††††††† Male††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 50 - 170 microgm/mL

††††††††††††††††††† Female†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 30 - 160 microgm/mL

LDH†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 105 - 230 U/L

Lipase, serum†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 16 - 63 U/L

Metanephrins, urine, adult

††††††††††††††††††† Metanephrine††††††††††††††††††††††††††††††††††††††††††††††††††††††† 0 - 300 microgm/gm of creatinine

††††††††††††††††††† Normetanephrine†††††††††††††††††††††††††††††††††††††††††††††††††† 0 - 400 microgm/gm of creatinine

Phosphorus††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 2.4 - 4.1 mg/dL

Plasma renin activity (upright)††††††††††††††††††††††††††††††††††††††††††††††† 0.5 - 3.3 ng/mL/hr

Potassium†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 3.7 - 5.2 mmol/L

Prostate specific antigen††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 0 - 4 ng/mL

Rheumatoid factor†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 0 - 20 IU/mL

Sodium††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 136 - 144 mmol/L

Thyroglobulin antibody†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 0 - 2 IU/mL

Thyroid peroxidase (TPO) antibody†††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 0 - 2 IU/mL

†† (antimicrosomal antibody)

Thyroid stimulating hormone (TSH)†††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 0.4 - 5 mU/L

Thyroxine††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 4.5 - 10.9 microgm/dL

T4, free††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 0.9 Ė 2.3 ng/dL

Total Protein, serum††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 6.3 - 8.2 g/dL

Total Protein, CSF†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 15 - 45 mg/dL

Troponin I†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† <0.4 ng/mL; >2 ng/mL consistent with myocardial injury

Urea Nitrogen (BUN)††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 7 - 20 mg/dL

Uric Acid†††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 2.7 - 6.6 mg/dL

 

Hgb†††††††††††††††††††††††††††††††† 12 - 16 g/dL††††††††††††††††††† female

†††††††††††††††††††††††††††††††††††††††† 13 - 18 g/dL††††††††††††††††††† male

Hct††††††††††††††††††††††††††††††††† 37 - 48 %††† female

†††††††††††††††††††††††††††††††††††††††† 42 - 52 %††† male

MCH†††††††††††††††††††††††††††††† 28 - 33 pg/cell

MCHC††††††††††††††††††††††††††† 32 - 36 g/dL

MCV†††††††††††††††††††††††††††††† 86 - 98 fL

RDW†††††††††††††††††††††††††††††† 11.5 - 14.5%

Platelets††††††††††††††††††††††††† 150,000 - 300,000/microliter

WBC count††††††††††††††††††† 4300 - 10,800/microliter

 

PT††††††††††††††††††††††††††††††††††† 12.5 seconds

PTT†††††††††††††††††††††††††††††††† 26.2 seconds

Fibrinogen 150 - 350 mg/dL

 

Lymphocyte subsets

††††††††††††††††††† CD4 cells (absolute)†††††††††††††††††††††††† 440 - 1600/microliter

††††††††††††††††††† CD8 cells (absolute)†††††††††††††††††††††††† 180 - 850/microliter

 

Quantitative Immunoglobulins

††††††††††††††††††† IgA††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 68 - 378 mg/dL

††††††††††††††††††† IgG††††††††††††††††††††††††††††††††† †††††††††††††††††††††††††††††††††††††††† 768 - 1632 mg/dL

††††††††††††††††††† IgM††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††††† 60 - 263 mg/dL

 

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