Friday, November 22, 2013

Nephronlithiasis

Renal colic
Epi dermiology and risk factor
10 % of population ( twice common in man )
Recurrence 50 % at 5 yrs
Peak incidence 30 -50 years of age

Clinical features

Urinary obstruction   upstream distention of ureter or  collecting  system  severe colicky pain
Writhing nerve comfortable .nausea vomiting.hematuria  (90%  microscopic) disphoresis .tachycardia. tachypnea
Occasionally gross symptomsof trigonal irritation (frequency.urgency )
Fever chills .rigors insecondary pyelonephritis

Differential diagnosis of renal colic

Acute uretheral obstruction (other causes )
UPJ obstruction sloughed papillae
Clot colic from gross hematuria
Extrinsic (eg tumour
Acute abdomen billary .bowel .pancrea.
Gynaecological –ectopic pregnancy.tortion rupture of ovarian cyst
Pyelonephritis (fever .chills .pyuria )
Radiculitis-herpes never root compression

Investigation

Screening lab
C B C_elevated W B Cin presence of fever suggest infection
Electrolyte Cr BUN_ toasses renal function
Urinary R &m ( WBC sRBC scrystal )C&S
Imaging
Non crystal spiral  CT is thestudy of choice
Abdominal ulterasoundmay demonstrate stone  or hydronephrosis
Interavenous pylogram (not used verymuch anymore
Strain all urine )stone analysis

Management

Analgesic.antimatic Iv fluidsurological consult is indicate.
Especially if stone <5mm has="" if="" infection="" o:p="" obstruction="" of="" or="" patient="" sign="">
A –blocker helpful to increase stone passage in select cases

Disposition


See admission criteria (sidebar ) most patientcanbe dischargeensure patient is stable .has adequate analgesia. And is able to tolerateoral meds. Follow up with family doctor in24 -48 hours 

Wednesday, October 9, 2013

Post Operative Care
pain management should be continuous from or to post-anesthetic unit to hospital ward and home 
pain service may assist with management of post operative inpatients.

Post-Operative nausea and Vomiting
more likely occur if young age female gender eye / middle ear / gynecological surgery, obese , history of post-anesthetic nausea / Vomiting.

Some anesthetic agents tend to cause more nausea post-operatively than other (e.g) opioids, nitrous oxide.

Hypertension and bradycardia must be ruled out. 

Pain/surgical manipulation also cause nausea.

Often treated with   dimenhydrinare (gravol.tm  ) metoclopramide (maxeran. tm) (not with bowel obstruction) prochlorperazine ( stematil ,tm) ondansetron (zofran.tm) granisetron.

post operative confusion and agitation .

ABCs first-confusion or agitation can be caused by airway obstruction, hypercapnea, hypoxemia.

Neurologic status (glassgow coma scale.pupils) residual paralysis from anesthetic.

Pain distended bowel /bladder.

Fear anxiety/separation from caregives/language barriers. 

Metabolic disturbance (hypoglycemia, hypercalcemia, hyponatremia-especially post TURP). 

Intracranial cause (stroke, raised intracranial pressure).

Drug effect (ketamine, anticholinergics).

Elderly patients are more susceptible to post-operative delirium. 

Sunday, October 6, 2013

Shoulder Dystocia

Definition

-Impaction of anterior shoulder of fetus against symphysis pubis after fetal head has been delivered
-Life threatening emergency

Etiology epidemiology

-Incidence 0.15-1.4% of deliveries
-Occurs when breadth of shoulder is greater than biparietal diameter of the head

Risk factor
-Maternal: obesity, Diabetes, multiparity
-Fetal: prolonged gestation, macrosomia

Labour :
-Prolong 2nd stage
-Prolonged deceleration phase (8-10 cm)
-Instrumental midpelvic delivery

Clinical feature
-“Turtle sign” (head delivered but retracts against inferior portion of pubic symphysis)

Complications:
Chest Compression by vagina or cord compression by pelvis can lead to hypoxia
Danger of brachial plexus injury (Erb palsy: C5-C7.klumpke;s palsy: C8-TI )
-90% resolve within 6 months
Fetal fracture (clavicle, humerus, cervical spine )
Maternal perineal injury, may result in PPH
Intrapartum fetal hypoxia of trauma

Treatment
Goal: to displace anterior shoulder from behind symphysis pubis; follow a stepwise approach of maneuvers until goal achieve (see box)

Other option when ALARMER fails :
-Cleidotomy (deliberate fracture of neonatal clavicle)
-Zavanelli maneuver: replacement of fetus into uterine cavity and emergent C/S
-Symphysiotomy
-Abdominal incision and shoulder disimpaction via hysterotomy - Subsequent vaginal delivery 

Prognosis
-90%of shoulder dystocias will resolve with McRobert’s maneuver and suprapubic pressure

-1%risk of long term disability for infant.

Wednesday, September 9, 2009

Pleural Effusion


  •   Pleural Effusion 

    Pleural effusion is an abnormal accumulation of fluid in the pleural space. The 5 major types of pleural effusion are transudates, exudates, empyema, hemorrhagic pleural effusion or hemothorax and chylous or chyliform effusion.
     Up to 25 ml of pleural fluid is normally present in the pleural space, an amount not detectable on conventional chest radiographs. 

     

    • The pleural cavity contains a small volume of lubricating serious fluid, formed primly by transudation from the pariental pleura and absorbed primarily by the capillaries and lymphatics . 


    pleural effusion develops when balance between formation and removal of fluid may be compromised by any disorder that 
     increases venous pressure
     lowers the plasma oncotic pressure.
     increases capillary permeability. 
     or obstruct the lymphatic circulation .

  General Considerations

Pleural effusions are classified as transudates or exudates to help in differential diagnosis.

 An exudates is a pleural fluid having one or more of the following features:
 pleural fluid protein to serum protein ratio> 0.5
 pleural fluid LDH to serum LDH ratio > 0.6
 pleural fluid LDH greater than two-thirds the upper limit of normal serum LDH.
 Transudates have none of these features 
 TRANSUDATES ARE CAUSED BY
 Decrease plasma oncotic pressure 
  >Nephrotic syndrome
  >Cirrhosis 
  >Hypoalbuminemia 
 Increased hydrostatic pressure
  >CHF
  >Superior vena cava obstruction 
 Exudates are caused by increased permeability of the pleural surface or by obstruction of the lymphatics .
 malignancy
  bronchogenic carcinoma 
  lymphoma
  metastatic tumor 
 inflammatory process
 infections:-
  - pneumonia
  - T.B
 - pulmonary embolism
 - collagen vascular disease (e.g. rheumatoid arthritis)  
 - Sub diaphragmatic process
 - asbestosis
 - pancreatitis
 - hypothyroidism 
 TRAUMA 

SYMPTOMS &SIGNS

 Small pleural effusions are usually asymptomatic 
whereas large pleural effusions may cause  
 Dyspnea Shortness of breath
 Fever
 Anorexia general malaise 
 Pleuritic pain
 Cough
 Haemoptysis
 Shortness of breath
 Night sweats 
   

 

Examination


 Decreased movement on the affected side
 Tracheal deviation, A massive pleural effusion with high intrapleural pressure may cause contra lateral shift of the trachea and bulging of the intercostals spaces 
 Stony dullness
 Decreased breath sound and vocal resonance
 Bronchial breathing aegophony 
 Look for underlying disease, clubbing ,tar, radiation mark L. Nodes, R.A.etc 


 LAB INVESTIGATIONS

Leukocytosis with bandemia

 PMN predominance:-

Pneumonia,PE, pancreatitis, early TB,abdominal abscess 

 Mononuclear predominance:-

  Tumors, TB.

 Eosinophil predominance;(40% of idiopathic effusions):
  Blood or air in the pleural space, asbestos, drugs, paragonimiasis 
 Eosinophil predominance reduces likelihood of TB (10x) and malignancy (2x)
 ANEMIA
  Pleurocrit/hematocrit >0.5 hemothorax 
 HYPOALBUMINEMIA
 ANTI NUCLEAR ANTI BODY TITER
  >1:160 OR> SERUM LEVEL:
  Suggests SLE effusion:
 RHEUMATIDE FACTOR>1:320 OR >SERUM LEVEL: SUGGESTS RHEUMATIOD ARTHRITIS
 PANCREATIC ENZMES
 CANCER ANTIGENS 125
 CANCER ANTIGEN 19-9
 CREATININE/ BLOOD UREA NITROGEN
 AEROBIC/ANAERBIC BLOOD/ PLEURAL FLUID CULTURES 

           Imaging

  •  CXR
  • anteroposterior or PA;
  • 75 ml to obliterate the posterior costophrenic sulcus 
  • 175ml to obscure the lateral costophrenic sulcus in erect position
  •  500ml will obscure the diaphragmatic contour , if reaches the level of the 4th anterior rib;close to 1000ml are present 

     



 


 

Massive pleural effusion (opacification of an entire hemi thorax) is usually caused by cancer but has been observed in tuberculosis and other diseases.

 


LATERAL VIEW :- 

Small effusion; thinner than 1.5 cm. Moderate ;1.5-4.5 cm thick. Effusion thicker than1cm is usually large enough for sampling by thoracentesis, at least 200ml.


 






Decubitus view


 

 Pleural fluid may become trapped (“loculated”) by pleural adhesions, forming unusual collections along the chest wall or in the lung fissures

 


THORACIC ULTRASOUND


 Ultrasound is useful to locate loculated or small effusions.

 

 




CT SCAN

 CT scanning is sensitive in the detection of small amounts of free or loculated pleural fluid. 

 

DIAGNOTIC PROCEDURES/ SURGERY

 Diagnostic thoracentesis is not required in small pleural effusion with secure clinical diagnosis or in patients with obvious CHF ,but consider in suspected CHF in following situations;
 -Unilateral effusion present ,particularly if it is left sided
 -bilateral effusion of disparate sizes
 -cardiac silhouette appears normal.
 Evidence of pleurisy 
 Febrile patient
 -Alveolar –arterial oxygen gradient is widened out of proportion of the clinical setting 

 

 



Contraindication for THORACENTESIS

 ANTICOAGULATION,BLEEDING DIATHESIS, PT PTT >x2normal ‘,Platelets <25000/mm3>6mg/dl,small pleural effusion,-mechanical ventilation, risk of persistent air leak –brocnchopleural fistula or pneumothoarax.

 -THORACOSCOPY provides direct view of both parietal and visceral aspects of pleura 

Initial laboratory tests for an undiagnosed pleural effusion


 Protein and LDH in pleural fluid and serum for separation of transudates and exudates
 Pleural fluid smears and culture
 Cell count and differential
 Pleural fluid glucose, amylase, pH
 Pleural fluid cytology
 Markers for TB pleuritis 
 ADA, gamma interferon or PCR 

EVALUATION OF PLEURAL FLUID WITH DRAWN BY THORACENTISIS


 TRANSUDATE has the protein content <30g/l>

 An exudate must meet also one the following criteria 

 >pleural fluid protein/serum protein >0.5

 >serum albumin-pleural albumin <1.2g/dl>

 >pleural fluid lactate dehydrogenase /serum lactate >0.6

 Pleural fluid lactate dehydrogenase exceeds 2/3 upper limit of that in serum 

Differential cell count


 Absolute cell count not very useful many diseases have WBC above 10,000

 Most transudates have WBC <1000>

 Differential -polys, small lymphocytes, other mononuclear cells and eosinophils 

 polys - acute process

 mononuclear cells - chronic process

 small lymphocytes - malignant, tuberculosis or post CABG pleural effusion

 eosinophils

Differential diagnosis of PMN predominant PE with acute infiltrate

 Tuberculous pleuritis 

 Pancreatic disease

 Postpericardiectomy syndrome

 Intra-abdominal abscess

 Viral pneumonia 

 Lung cancer with pleural effusion

 Pulmonary embolism

 Lupus pleuritis 

 Rheumatoid pleural effusion

 Drug reaction

Pleural fluid eosinophilia (>10%)

 Usually due to air or blood in the pleural space
 Consider drug reactions
 Dantrolene, bromocriptine, nitrofurantoin 
 Frequent with asbestos pleural effusion
 Rarely paragonimiasis or Churg-Strauss syndrome
 also low glucose and pH
 Frequently no diagnosis obtained


COMPREHENSIVE MICROBIOLOGICAL CULTURING AND GRAMSTAINING /FOR AFB CULTURE AND STAINING.

 The Pleural fluid should be evaluated for aerobic and anaerobic bacteria ,mycobacteria ,protoza ,fungi and parasites 

Pleural fluid LDH


 Not useful in the differentiation of exudates because all exudates tend to have elevated LDH
 Very useful when following a patient with a pleural effusion because the level of pleural fluid LDH reflects degree of pleural inflammation
 If LDH worsens with serial thoracentesis, process is worsening and one should be more aggressive
 If LDH decreases with serial thoracenteses, process is improving

Differential diagnosis -low glucose (<40mg/dl)

 Complicated Para pneumonic effusion

 Malignant pleural effusion

 Tuberculous pleural effusion

 Rheumatoid pleural effusion

 Paragonimias 

 Hemothorax 

 Churg-Strauss syndrome

 <30mg/dl>

 <60mg/dl>

Differential diagnosis of high amylase pleural effusion; increased

 Acute pancreatic disease

 Chronic pancreatic disease

 Pancreatic pseudo-cyst

 Esophageal rupture

 Malignant pleural effusion

Pleural fluid pH

 Particularly useful in patients with suspected parapneumonic effusion

 pH <>

 Low pH (<7.2)>

 Must be measured with blood gas machine 

Pleural fluid markers for tuberculosis

 Adenosine deaminase (ADA)   >T-lymphocyte enzyme

  >Patients withTB have levels above 45 IU/L unless they are immunologically suppressed
  >High levels also seen with empyema and rheumatoid pleuritis 
  >Specificity increased if combined with PF lymph/poly ratio greater than 3  
 Gamma interferon
  >Produced by lymphocytes
  >Lymphocytes specifically sensitized to PPD produce gamma interferon when incubated with PPD
  .PF levels above 140pg/ml are very suggestive of TB
  >Elevated whether or not the patient is immunosuppressed 
  >Is more expensive than ADA

PCR for DNA of M. tuberculosis


 If pleural fluid ADA >70 units - diagnostic
 If pleural fluid gamma interferon is high - diagnostic
 Granulomas on pleural biopsy - diagnostic
 If lymphocytic effusion and positive PPD, treat for TB pleuritis if pleural fluid ADA is above 40
 If lymphocytic effusion and negative PPD, retest the PPD in 5 weeks - treat if positive 

Pleural fluid cytology


 Very useful test
 1st specimen positive in 60% and if three specimens submitted, may be positive in >80%
 Very effective with adenocarcinoma 
 Less effective with lymphoma, squamous cell carcinoma, mesothelioma or Hodgkin’s disease 
 Flow cytometry Very useful for demonstrating homogeneity of cells with lymphoma
 Immunohistochemical studies ;Monoclonal antibodies are made against various antigens that are thought to be specific for adenocarcinoma, benign mesothelial and malignant mesothelial cells
 Diagnostic techniques for tumor markers; There have been many studies evaluating the utility of tumor markers such as CEA, CA 15-3, CA 19-9, and enolase 
 Collagen vascular disease;
  > Rheumatoid pleuritis - useful easy to diagnose
  -patient elderly man with rheumatoid nodules
  -pleural fluid - low glucose, high LDH, low pH
  -must differentiate from complicated parapneumonic 
 Lupus erythematosus -more difficult
  -pleural fluid ANA -probably add little to serum ANA 

Chylothorax and pseudochylothorax

 with pseudochylotorax, effusion has been present for years and pleura is markedly thicked 

 with chylothorax, an acute process
 If doubt, measure triglycerides and cholesterol in serum and pleural fluid. Chylothorax exists if:
 Triglycerides >110 mg/dl and

 Pleural fluid/serum triglyceride >1.0Pleural fluid/serum cholesterol <1.0>

PLEURAL BIOPSY if suspicion of TB or NEOPLASM

Closed pleural biopsy should be considered in the differential diagnosis of a pleural effusion that is unexplained after routine studies and thoracentesis. Contraindications include bleeding diathesis, poor respiratory reserve, empyema and absence of pleural fluid.

Open pleural biopsy is sometimes required to establish the diagnosis of pleural malignancy and is especially indicated for the diagnosis of malignant pleural mesothelioma.

Thoracoscopy with a flexible instrument is an alternative procedure with excellent diagnostic accuracy 

Treatment

 INITIAL STABILIZATION;

 Inpatient care is required with this condition.

 GENERAL MEASURES 

 SUPPLEMENTAL OXYEGEN to keep saturation in normal range.

 IV Fluid for hydration.  Chest physiotherapy.

 THERAPEUTIC /DIAGNOSTIC THORACENTESIS. 

 Treatment should address both the disease causing the pleural effusion and the effusion itself.  Transudative Pleural Effusion.

 Transudative pleural effusions generally respond to treatment of the underlying condition; therapeutic thoracocentesis is indicated only if massive effusion causes dyspnea. 

 When bilateral pleural effusions are detected with congestive heart failure, neither diagnostic nor therapeutic thoracentesis is routinely indicated. Such effusions are transudates and will resolve with treatment of the underlying cardiac disease.

ANTIBIOTICS

Empirically by age/social circumstances and modified by blood and pleural fluid culture results.

Empyema ; Antibiotics alone with  close monitoring in children. Antbiotics with chest tube drainage in adults.PLEURECTOMY;in cases of trpped lung

 Pleural fluid loculation    > May inject 250,000 units of streptokinase or hundred thousand units of urokinase intrapleurally to dissolve fibrin meshes creating loculation. If unsuccessful, then either thoracoscopic adhesiolysis or decortication via thoracotomy is indicated.

 Malignancy consider treatment of primary source-chemotherapy.
 If effusion is causing dyspnea perform therapeutic thoracentesis, if fluid reaccumulates rapidly place chest tube for continious drainage or chemical pleurodesis with doxy cycline 500 mg, bleomycine 60 units are talc. If pleurodesis fails pleural aberation can be done or pleuroperitoneal shunt and chemical pleurodysis 

 Chylothorax 
  >radiation therapy if from malignant cause or surgical repair of thoracic duct trauma.
 Hemothorax 
  > usually caused by trauma or rupture of a tumor drainage through tube thoracostomy.
 Steroids and NSAIDs for rheumatological and inflammatory causes 
 Diuresis for CHF and ascites  


Complications


 Chronic empyema 
 Drainage through chest wall: Peurocutaneous fistula
 Broncho pleural fistula 
 Toxic shock syndrome 

 
This article is prepared by Dr Muhammed Naeem Awan

Sunday, September 6, 2009