mlt clinical case study

25
Anneka Pierzga MLT 2015 Professor Tiffany Gill December 12 th , 2016 College of Southern Maryland CLINICAL CASE STUDY

Upload: anneka-pierzga

Post on 14-Apr-2017

17 views

Category:

Health & Medicine


1 download

TRANSCRIPT

Page 1: MLT Clinical Case Study

Anneka PierzgaMLT 2015Professor Tiffany GillDecember 12th, 2016College of Southern Maryland

CLINICAL CASE STUDY

Page 2: MLT Clinical Case Study

History and presentation

The Patient

Page 3: MLT Clinical Case Study

68 year old Caucasian male Hx: Peripheral vascular disease

Atrial fibrillation, hypertension, hyperlipidemia, benign prostatic hypertrophy Smoking (75 pack/year) Chronic alcohol consumption Denies history of MI, but does have a familial history of myocardial infarction Denies history of diabetes mellitus

14 months post R popliteal artery bypass graft

The Patient

Page 4: MLT Clinical Case Study

Current medications Aspirin 81mg PO QD (antiplatelet/anticoagulant) Atorvastatin (Lipitor) PO QD (hyperlipidemia) Plavix PO QD (antiplatelet/anticoagulant) Losartan PO QD (hypertension) Metoprolol PO QD (hypertension) Pentoxifylline PO QD (anti-inflammatory and vasodilator) Tamsulosin PO QD (for treatment of urinary retention in BPH) Rivaroxaban (anticoagulant) Folic acid QD

The Patient

Page 5: MLT Clinical Case Study

Allergies Iodine Penicillin

The Patient

Page 6: MLT Clinical Case Study
Page 7: MLT Clinical Case Study
Page 8: MLT Clinical Case Study

Physical exam 2 week history of numbness/coolness of the surgical limb

Extremities: both legs cool to the touch Feet: pink with CRT

No evidence carotid bruits Femoral pulses slow R leg, WNL on L Pedal pulses absent bilaterally

Presentation

Page 9: MLT Clinical Case Study

Diagnosis, plan and treatment

Putting it together

Page 10: MLT Clinical Case Study

Diagnosis on Admission1. Subacute occlusion of the R femoral popliteal bypass graft for 11 days!2. Ischemic leg3. Dyslipidemia4. Atrial fibrillation5. Benign prostatic hypertrophy

Putting it together

Page 11: MLT Clinical Case Study

Plan Admission with STAT CT/Angiogram Transluminal angioplasty with placement of a stent Anticoagulant therapy

Putting it together

Page 12: MLT Clinical Case Study

Treatment

Angioplasty and stent placement: https://www.youtube.com/watch?v=veP5R-pzJVk

Page 13: MLT Clinical Case Study

Post-operative medications TPN (nutritional support) Famotidine PO (gastroprotectant) Lipitor PO (hyperlipidemia) Metoprolol PO (beta blocker) Tamsulosin PO (treat urinary retention) Hydromorphone IV (pain management) Lorazepam IV (sedative and anxiolytic) Heparin IV (anticoagulant)

Treatment

Page 14: MLT Clinical Case Study

Labwork

UA CBC CMP/BMP Coagulation studies

Page 15: MLT Clinical Case Study

Specimen 1Date:11/19/16Time: 11:35am

Analyte Test Results

Color yellow

Clarity clear

Specific Gravity 1.016

Glucose negative

Bilirubin Negative

Ketones Negative

Urinalysis

Blood Negative

Ph 6.0

Protein Negative

Urobilinogen < 2.0 mg/dL

Nitrite Negative

Leukocyte Esterase Negative

Unremarkable; microscopic examination not performed

Page 16: MLT Clinical Case Study

CBCCBC Laboratory Results

Analyte Specimen 1Date: 11/18/16 Time: 11:54am

Specimen 3Date:11/21/16 Time:17:59p

Specimen 5Date:11/22/16

Time:4:40a

Specimen 7Date:11/23/16

Time:6:03a

WBC (x103/mcL) 7.5 4.7 6.0 9.3RBC (x106/mcL) 4.88 3.5L 4.07L 4.00L

Hgb (g/dL) 17.3H 12.4L 14.2 13.8Hct (%) 48.9 36.3L 41.5 40.2

MCV (fL) 100.2 103.7H 102.0 100.5MCH (pg) 35.5H 35.4H 34.9H 34.5H

MCHC (g/dL) 35.4 34.2 34.2 34.3RDW (%) 12.9 12.9 12.8 12.7

Platelets (x103/mcL) 177 77L 100 123L

Neutrophils (x103/mcL) 5.3 3.9 4.9 6.8Lymphocytes (x103/mcL) 1.6 0.5L 0.7 1.5Monocytes (x103/mcL) 0.6 0.3 0.4 0.9Eosinophils (x103/mcL) 0.1 0 0 0Basophils (x103/mcL) 0 0 0 0

Page 17: MLT Clinical Case Study

CBC Interpretation

Thrombocytopenia due to anticoagulant therapy Anemia (decreased hematocrit, Hgb) day of surgery, likely due

to bleeding during surgery Increased MCH – macrocytosis, possible that patient had

been taking Folic acid supplements for management of a megaloblastic anemia due to folate deficiency from chronic alcoholism?

Page 18: MLT Clinical Case Study

CMPCMP Laboratory Results

Analyte Specimen 1Date: 11/18/16 Time:

11:54am

Specimen 4Date: 11/22/16 Time:_ 4:40a

Specimen 6Date:11/23/16

Time:6:03p

Specimen 7Date:_11/23/16 Time:16:00

Specimen 8Date:_11/26/16 Time:4:30a

Glucose (mg/dL)

96 140H 87 80 98

BUN (mg/dL) 7 11 11 9 7

Creatinine (mg/dL)

0.80 0.74 0.79 0.79 0.87

Na (mmol/L) 142 146H 145 145 137

K (mmol/L) 4.5 3.6 2.9L 3.3L 3.9

Cl (mmol/L) 104 106 102 102 97L

Total CO2 (mmol/L)

29.0 32.0 35.0H 38.0H 31.0

Ca (mg/dL) 9.3 6.7L 6.8L 6.4L 7.8L

Total Bili (mg/dL)

0.8 0.4 0.6 0.5 0.8

Direct Bili Not performed Not performed Not performed Not performed Not performedTotal Protein

(g/dL)8.0 5.1L 5.2L 4.8L 5.3L

Albumin (g/dL)

3.9 2.2L 2.3L 2.0L 1.9L

ALP (U/L) 97 47 49 46 121H

AST (U/L) 48H 481H 397H 340H 165H

ALT (U/L) 37 74H 73H 64H 53H

Page 19: MLT Clinical Case Study

Other TestsOther Test Results

Specimen 4Date:

11/22/16 Time:_ 4:40a

Specimen 6Date:11/23/

16 Time:6:03p

Specimen 7Date:_11/23/16

Time:16:00

Specimen 8Date:_11/26/16

Time:4:30a

Magnesium (mg/dL)

2.7H 2.3 2.0 1.8

Ammonia (mcmol/L)

43H 38H 50H

Total CK (U/L)

111728H 3132H

Page 20: MLT Clinical Case Study

CMP Interpretation

Evidence of alcoholic hepatitis, possibly cirrhosis? ↑↑ AST>ALT, hyperammonemia, hypoalbuminemia, hypomagnesemia, hypocalcemia – abnormalities could be exacerbated by alcohol withdrawal

Elevated total CK likely due to recent surgical manipulation of tissues (no reports of chest pain or other to suggest AMI, and no CK-MB/Troponin I ordered)

Transient hyperglycemia – possibly stress related, as patient had denied a history of DM. Could also be post-prandial samples. Patient had been receiving TPN could cause hyperglycemia

Page 21: MLT Clinical Case Study

CoagulationCoagulation Laboratory Results

Analyte Specimen 1Date:11/21/16

Time:1:55a

Specimen 2Date:11/21/16_

Time:17:59p

Specimen 3Date:11/22/16

Time:0:13a

Specimen 5Date:11/23/16

Time:6:03a

Specimen 7Date:

11/24/16 Time:5:19a

Specimen 8Date:11/25/16

Time:5:40a

PT (sec) 14.7H 15.2H 13.0H 12.0 Not performed

18.5H

PTT (sec) 31.5H 36.9H 29.7H 26.7 Not performed

Not performed

Anti-Xa (IU/mL)

Not performed Not performed Not performed 0.56 0.55 0.63

INR 1.40 1.44 1.24 1.15 NP 1.75

Page 22: MLT Clinical Case Study

Coagulation Studies Interpretation

Monitoring of coagulation parameters seems to have started after initiation of heparin therapy, so unsure of what coagulation status was prior to this. Patient has been on aspirin and rivaroxaban for some time prior to admission (aspirin causes decreased platelet aggregation and increased bleeding time, rivaroxaban inhibits factor Xa). Patient also appears to have alcoholic liver disease, which may also affect coagulation studies (usually by prolongation of PT)Patient was treated with heparin therapy during hospitalization, which can produce prolongation of both the PT and PTT, although the PTT is a more sensitive measure of heparin effect. Heparin also inactivates factor Xa, and over the course of the patient’s hospitalization, we see his measured anti-Xa fall into the laboratory defined therapeutic range of 0.3-0.7IU/mL as therapeutic for treatment of DVT/A-Fib

Page 23: MLT Clinical Case Study

Prognosis and recommendations

Prognosis

Page 24: MLT Clinical Case Study

Admitted 11/18, discharged 11/30 At discharge, patient appeared to be doing well with good evidence of

revascularization of the affected limb Patients with symptomatic peripheral vascular disease tend to have

poor long-term prognosis Cease smoking and alcohol intake Exercise, improve dietary habits

Prognosis

Page 25: MLT Clinical Case Study

American Heart Association. (2016). What is Atrial Fibrillation? Retrieved from http://www.heart.org/HEARTORG/Conditions/Arrhythmia/AboutArrhythmia/What-is-Atrial-Fibrillation- AFib-or-AF_UCM_423748_Article.jsp#.WE4Vw1wW5s4Conejero, A. M., & Hernando, F. J. S. (2007). Peripheral Artery Disease: Pathophysiology, Diagnosis and Treatment. Revista Española De Cardiología, 60(9), 969-982. Eltzschig, H. K., & Collard, C. D. (2004). Vascular Ischaemia and Reperfusion injury. British Medical Bulletin, 70(1), 71-86. Johns Hopkins Medicine Health Library. (2016). Fmoral Popliteal Bypass Surgery. Retrieved from http://www.hopkinsmedicine.org/healthlibrary/test_procedures/cardiovascular/femoral_popliteal_bypas s_surgery_92,p08294/Lau, Y. F., Siu, C. W., Tse, H. F., & Yiu, K. H. (2012). Hypertension and Atrial Fibrillation: Epidemiology, Pathophysiology and Therapeutic Implications. Journal of Human Hypertension, 26, 563-569. MedicalExhibits. (2016). Femoral-Popliteal Bypass Surgery: Medical Exhibits, Demonstrative Aids, Illustrations and more.Mosquera, D. (2013). Angiogram and Angioplasty.National Heart, L., and Blood Institute,. (2016). What are the Signs and Symptoms of Carotid Artery Disease? Retrieved from https://www.nhlbi.nih.gov/health/health-topics/topics/catd/signsNational Heart, L., and Blood Institute. (2016). Smoking and Atherosclerosis.Pierce, S. M. (2016). Acute Lower Extremity Compartment Syndrome. Retrieved from http://nurse- practitioners-and-physician-assistants.advanceweb.com/Continuing-Education/CE-Articles/Acute-Lower-Extremity- Compartment-Syndrome.aspxSantilli MD, J. D., & Steven M. Santilli, M., PHD. (1991). Chronic Critical Limb Ischemia: Diagnosis, Treatment and Prognosis. American Family Physician, 59(7), 1899-1908. StockUnlimited. (2016). Medical Clipboard.

References