TWO CASES WITH HEMOPTYSISTWO CASES WITH HEMOPTYSISCASE 2CASE 2
PROF.S.SUNDAR’S UNIT
Dr.V.Jayaprakash
Mr.Marimuthu, Mr.Marimuthu, 35 years,lorry driver,admitted on 12.2.200935 years,lorry driver,admitted on 12.2.2009
C/O Breathlessness – 1 day
H/O Presenting illness:• The patient was apparently alright 1 day back when he
developed acute onset of breathlessness,stationary in course,class 4,aggravated by exertion and relieved by rest and sitting posture
• H/O orthopnea• No H/O chest pain• No H/O palpitation/syncope/pedal edema
• No H/O cough/hemoptysis/wheeze• No H/O fever• No H/O abdominal pain/abdominal distension/oliguria• No H/O swelling of legs
PAST H/O:• No H/O of similar illness in the past• No H/O recent surgery/travel/immobility• No H/O DM/SHT/bronchial asthma/TB/CAHD/CVA/
seizure disorder• H/O vascular disease of right lower limb 5 years back for
which he had undergone bypass surgery
PERSONAL HISTORY:
• Mixed diet
• Smoker for 10 years; smokes one pack per day
• Occasionally consumes alcohol
FAMILY HISTORY:
• Nil significant
TREATMENT HISTORY:
• Nil significant
GENERAL EXAMINATIONGENERAL EXAMINATION
Conscious Oriented Afebrile No pallor Central cyanosis No clubbing Dyspneic and tachypneic No pedal edema/calf muscle tenderness No generalised lymphadenopathy BP – 110/80 mmHg PR – 120/minDorsalis pedis and posterior tibial pulsation absent in both lower limbs RR – 35/min JVP – Not elevated
• CARDIOVASCULAR SYSTEM: S1S2 heard No murmurs• RESPIRATORY SYSTEM: NVBS heard No added sounds• ABDOMINAL EXAMINATION: Soft Midline scar+ No organomegaly/ Free fluid• CENTRAL NERVOUS SYSTEM: No focal neurological deficit
PROVISONAL DIAGNOSISPROVISONAL DIAGNOSIS
ACUTE BREATHLESSNESS FOR EVALUATION
? Pulmonary Thromboembolism
No evidence of DVT clinically
INVESTIGATIONSINVESTIGATIONS
Urine routine – Normal
CBC:
Hb – 13 g%
TC – 12000
DC – P85 L16 E4
ESR – 5/12
PCV – 42%
Platelet – 1.2 lakh
Blood sugar ®- 107mg%
Urea – 27 mg%
Sr creatinine – 0.8 mg%
Sr Na+ - 140 mmol/l
K+ - 4.1 mmol/l
Sr Lipid profile – 186 mg%
ECG on admissionECG on admission
Chest X ray PA viewChest X ray PA view
• CHEST X RAY PA VIEW
Prominent pulmonary artery
• ECG
Sinus tachycardia
RBBB
S1 Q3 T3 pattern
ST segment depression in lead I and ll
ST segment depression in left precordial leads
Tall R waves in right precordial leads
ECG FINDINGS IN PULMONARY EMBOLISMECG FINDINGS IN PULMONARY EMBOLISM
• Low amplitude deflection• Right atrial enlargement• Right ventricular hypertrophy• Right ventricular myocardial ischemia• Right ventricular myocardial injury• RBBB• Atrial tachyarrythmias
ECG FINDINGS IN PULMONARY EMBOLISMECG FINDINGS IN PULMONARY EMBOLISM
FRONTAL PLANE LEADS: S1Q3T3 pattern ST segment depresson in standard lead l and ll Right axis deviation Tall peaked T wave in lead ll
HORIZONTAL LEADS: T wave inversion in right precordial leads ST segment elevation in right precordial leads ST segment depression in left precordial leads Increase in R amplitude in right precordial leads RBBB
• ECHOCARDIOGRAM: No RWMA Normal LV systolic function TR mild TRPG 48 mmHg Mild RA/RV dilated
• D-DIMER LEVEL: 3.27 microgram/ml – POSITIVE (Normal : < 0.5 mcg/ml)
FURTHER INVESTIGATIONSFURTHER INVESTIGATIONS
• CT Chest – Normal study• Doppler study of both lower limbs – No evidence of DVT• Lupus anticoagulant – Negative• Anti CardioLipin Antibody (ACLA) – Normal IgG – 5.11 GPLU/ml (Normal - < 10) IgG – 3.65 mPLU/ml (Normal - <7)• Protein C levels – 44.6% (Normal :70 – 140%) • Protein S levels – 39.7% (Normal : 60 – 150%)• Sr homocysteine level – 20.31 mcmol/l (Normal:5.9 – 16)• Antithrombin levels – Not done• Factor V Leiden – Not done
15/2/09 18/2/09 23/2/09 PT 17.6 26.3 24.2 aPTT 36.4 40 40.5 INR 1.6 2.8 2.68
FINAL DIAGNOSISFINAL DIAGNOSIS
PULMONARY THROMOEMBOLISM
PROTEIN C DEFICIENCY
PROTEIN S DEFICIENCY
NO DEEP VENOUS THROMBOSIS
TREATMENT GIVENTREATMENT GIVEN
• Supportive measures
• Unfractionated Heparin
• Acenocoumarol
• Folic acid tablets
• B – complex supplements
VENOUS THROMBOEMBOLIC DISORDERS (DVT & PE)VENOUS THROMBOEMBOLIC DISORDERS (DVT & PE)
• ETIOLOGY:ETIOLOGY: Stasis, Hypercoagulability, Venous endothelial injury
• STASIS: Immobilisation (Trauma,Surgery,Immobilisation)
• HYPERCOAGULABLE STATES:• Inherited: Prothrombin gene mutation, partial protein C
deficiency, partial protein S deficiency, partial antithrombin deficiency,factor V Leiden, hyperhomocystinemia
• Acquired: Malignancy, nephrotic syndrome, estrogen use, pregnancy, HIT,APA syndrome, sickle cell disease, marrow fat embolism, amniotic fluid embolism
CLINICAL PRESENTATIONCLINICAL PRESENTATION (Signs and symptoms of DVT & PE are neither sensitive nor specific)(Signs and symptoms of DVT & PE are neither sensitive nor specific)
CLINICAL DECISION RULES:
Clinical variable Score
• Signs and symptoms of DVT 3.0• Alternative diagnosis less likely than PE 3.0• Heart rate >100/min 1.5• Immobilisation>3 days,Surgery within 4 wks 1.5• Prior PE or DVT 1.5• Hemoptysis 1.0• Cancer 1.0
High clinical likelihood of PE if the point score exceeds 4.0
ASSESSMENT OF SEVERITY OF PEASSESSMENT OF SEVERITY OF PE
MASSIVE PE: • Systemic Arterial Hypotension
MODERATE TO LARGE PE:• RV Hypokinesias in Echocardiography• Normal Systemic Arterial Pressure
SMALL TO MODERATE PE:• Normal Right Heart Function• Normal Systemic Arterial Pressure
LABORATORY STUDIESLABORATORY STUDIES
D-DIMER:
• Cross linked fibrin degradation product that may be increased during acute illness or VTE.
• It has a low positive predictive value and specificity – If positive, requires further evaluation.
• It has high negative predictive value-If negative,it excludes DVT.
LABORATORY ASSESSMENT OF INHERITED LABORATORY ASSESSMENT OF INHERITED THROMBOPHILIC STATESTHROMBOPHILIC STATES
Prothrombin gene mutation G20210A
G20210A mutation
Partial protein C deficiency
Partial protein S deficiency
Protein C activity
Protein S activity,
Free protein S antigen
Factor V Leiden Activated protein C resistance, if positive confirm with Factor V Leiden PCR
Hyperhomocystinemia Fasting plasma homocysteine levels
LABORATORY ASSESSMENT OF LABORATORY ASSESSMENT OF ACQUIRED THROMBOPHILIC STATESACQUIRED THROMBOPHILIC STATES
ANTIPHOSPHOLIPID ANTIBODY SYNDROME
LUPUS ANTICOAGULANT,
ANTICARDIOLIPIN ANTIBODY,
BETA 2 GLYCOPROTEIN 1
PNH RBC OR WBC FLOW CYTOMETRY FOR LOSS OF CD55,CD59
MYELOPROLIFERATIVE DISORDER
JAK – 2 MUTATION
IMAGING - DVT SPECIFIC TESTINGIMAGING - DVT SPECIFIC TESTING
• Duplex Examination -
Compressive ultrasound performed with doppler testing
• Venography
• MRI
• CT Venography
PEPE SPECIFIC TESTING SPECIFIC TESTING
NONSPECIFIC TESTS:
~ ECG,Troponin levels, Chest Radiography
~ Determine pretest probability of PE along with D-Dimer assay
CONTRAST ENHANCED SPIRAL(HELICAL) CHEST CT:
~ Relatively accurate for large(proximal) PE, but sensitivity is low for small(distal) emboli
~ Clinical suspicion that is discordant with the objective finding should lead to further testing
V/Q SCANNING: Requires administration of radioactive material(via both inhaled and
i.v. routes) V/Q scan can be classified as normal, non diagnostic or high
probability for PE Use of clinical suspicion improves the accuracy of V/Q scan When both the findings are discordant, further testing should be
performed
MR ANGIOGRAPHY
PULMONARY ANGIOGRAPHY
TREATMENTTREATMENT
UNFRACTIONATED HEPARIN (UFH):
• 80 U/kg bolus followed by infusion of 18 U/kg/hr.• Continued for atleast 4-5 days and until INRs of atleast 2 are achieved on 2
consecutive days with warfarin therapy.
LMWH:
VKAs(Vitamin K Antagonists), Warfarin or Acenocoumarol:
• Started as 5 mg PO and dose adjusted according to INR• INR should be done frequently during the first month,because multiple dose
adjustments are usually necessary to achieve therapeutic INR• Once a stable dose is achieved, INR monitoring should be done atleast 4
weeks.
• THROMBOLYTIC THERAPY- INDICATIONS:
Refractory Systemic Hypotension
? Right Ventricular Dysfunction
• ANTITHROMBIN III INFUSION:
In patients with congenital antithrombin lll deficiency - during an acute thromotic episode
INVASIVE SPECIAL THERAPIESINVASIVE SPECIAL THERAPIES
• IVC FILTERS:
1] Acute DVT states in which there is absolute contraindication to anticoagulation
2] Recurrent thromboembolic episodes
• CATHETER EMBOLECTOMY
• SURGICAL EMBOLECTOMY
LONG TERM TREATMENT WITH VITAMIN K LONG TERM TREATMENT WITH VITAMIN K ANTAGONISTS FOR DVT AND PEANTAGONISTS FOR DVT AND PE
First episode of DVT or PE secondary to a transient risk factors
3 mon Recommendation applies to both proximal and calf vein thrombosis
First episode of idiopathic DVT or PE
6 – 12 mon
Continuation of therapy after 6 -12 mon to be considered
First episode of DVT or PE with a documented thrombophilic abnormality
6 – 12 mon
Continuation of therapy after 6 -12 mon to be considered
First episode of DVT or PE with documented antiphospholipid or >= 2 thrombophilic abnormality
12 mon
Continuation of therapy after 12 mon to be considered
COURSE OF THE ILLNESSCOURSE OF THE ILLNESS
His breathlessness improved, was able to walk about 100 m without breathlessness. Except for sinus tachycardia, ECG features of PE disappeared. He was discharged at request on 27.2.2009 with advice to continue acitrom and to get readmitted after 3 days for planning CT Angiogram. But he came for admission the next day itself with massive hemoptysis; cause - ?acitrom related ?massive pulmonary embolism and infarct. He was treated with vitamin K, FFP and blood transfusion; shifted to IMCU for intensive care. Evaluation revealed prolonged coagulation parameters. PT- 48 seconds, INR- 4.3. Massive hemoptysis recurred and the patient had hypoxia and altered sensorium. Despite the best possible efforts, the patient succumbed to his illness.
ACKNOWLEDGEMENTSACKNOWLEDGEMENTS
• THE PATIENT AND HIS FAMILY
• IMCU TEAM
thank you
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