Saturday, December 19, 2009

65 - Hypertrophic Pyloric stenosis

The majority of infants vomit. Because infant vomiting is so common, it is important to differentiate between normal vomiting—as occurs in almost all infants, to some degree—and abnormal vomiting, which may be indicative of a potentially serious underlying disorder. The color of the emesis and the child's overall condition must be assessed. Vomit that looks like feeds and comes up immediately after a feeding is almost always gastroesophageal reflux. This may or may not be of concern, as described earlier. Vomiting that occurs a short while after feeding, or indeed vomiting that projects out of the baby's mouth, may be indicative of pyloric stenosis. By contrast, vomit that has any green color in it is always worrisome. This may be reflective of intestinal volvulus, an underlying infection, or some other cause of intestinal obstruction.


Clinical Manifestations :

The ability to provide timely diagnosis and treatment of infants with hypertrophic pyloric stenosis (HPS) is another milestone in the history of pediatric surgery. HPS occurs in approximately 1 in 300 live births and originally was believed to occur in first-born males between 3 and 6 weeks of age. Subsequent studies determined that this was a statistical error; investigators did not account for the incidence of first-born males as a group. However, children with HPS outside of this age range are commonly seen, and the cause of HPS has not been determined. Studies have shown that HPS is found in several generations of the same family, which suggests a familial link. Administration of erythromycin in early infancy was also thought to be linked to the subsequent development of HPS, but rates of HPS have not decreased with the decline in the use of erythromycin, so this may also have been an erroneous conclusion.

Infants with HPS present with nonbilious vomiting that becomes increasingly projectile over the course of several days to weeks. Eventually, the infant develops almost complete gastric outlet obstruction and is no longer able to tolerate even clear liquids. Despite the recurrent emesis, the child normally has a voracious appetite, which leads to a cycle of feeding and vomiting that invariably results in severe dehydration if the condition is untreated. Jaundice may occur in association with HPS, although the reason for this is unclear. Particularly perceptive caregivers will mention that the infant is passing less flatus, which provides a further clue that gastric outlet obstruction is complete.

Infants with HPS develop a hypochloremic, hypokalemic metabolic alkalosis. The urine pH is high initially but eventually drops because hydrogen ions are preferentially exchanged for sodium ions in the distal tubule of the kidney as the hypochloremia becomes severe. The diagnosis of pyloric stenosis usually can be made on physical examination by palpation of the typical "olive" in the right upper quadrant and the presence of visible gastric waves on the abdomen. When the olive cannot be palpated, ultrasonography can diagnose the condition accurately in 95% of patients. Criteria for ultrasonographic diagnosis include a channel length of greater than 16 mm and pyloric thickness of greater than 4 mm.

Treatment :

Pyloric stenosis is never a surgical emergency, although the dehydration and electrolyte abnormalities may present a medical emergency. Fluid resuscitation with correction of electrolyte abnormalities and metabolic alkalosis is essential before induction of general anesthesia for operation. For most infants, administration of fluid containing 5% dextrose and 0.45% saline with 2 to 4 mEq/kg of added potassium at a rate of approximately 150 to 175 mL/kg for 24 hours will correct the underlying deficit. It is important to ensure that the child has an adequate urine output (greater than 1 mL/kg per hour) as further evidence that rehydration has occurred. After resuscitation, a Fredet-Ramstedt pyloromyotomy is performed. The procedure may be performed using an open or laparoscopic approach. Open pyloromyotomy is performed through either an umbilical or a right upper quadrant transverse abdominal incision. The former route is cosmetically more appealing, although the transverse incision provides easier access to the antrum and pylorus. In recent years, the laparoscopic approach has gained great popularity. Two randomized trials have demonstrated that both the open and laparoscopic approaches may be performed safely with equal incidence of postoperative complications, although the cosmetic result is definitely superior after the laparoscopic approach. Whether performed using an open or laparoscopic approach, surgical treatment of pyloric stenosis involves splitting the pyloric muscle until the submucosa bulges upward. The incision begins at the pyloric vein of Mayo and extends onto the gastric antrum; it typically measures between 1 and 2 cm in length. Postoperatively, IV fluids are continued for several hours, after which an oral electrolyte solution (Pedialyte) is offered, followed by formula or breast milk, which is gradually increased to 60 mL every 3 hours. Most infants can be discharged home within 24 to 48 hours after surgery. Recently, several authors have shown that ad lib feedings are safely tolerated by the neonate and result in a shorter hospital stay.

The complications of pyloromyotomy include perforation of the mucosa (1 to 3%), bleeding, wound infection, and recurrent symptoms due to inadequate myotomy. When perforation occurs, the mucosa is repaired with a stitch that is placed to tack the mucosa down and reapproximate the serosa in the region of the tear. A nasogastric tube is left in place for 24 hours and taped securely to prevent it from reinjuring the repaired mucosa. The outcome is generally very good.

64 - Exudative Pleural Effusion causes


 Exudative pleural effusions
  A. Neoplastic diseases
    1. Metastatic disease
    2. Mesothelioma
    3. Body cavity lymphoma
    4. Pyothorax-associated lymphoma
  B. Infectious diseases
    1. Tuberculosis
    2. Other bacterial infections
    3. Fungal infections
    4. Parasitic infections
    5. Viral infections
  C. Pulmonary embolization
  D. Gastrointestinal disease
    1. Pancreatic disease
    2. Subphrenic abscess
    3. Intrahepatic abscess
    4. Intrasplenic abscess
    5. Esophageal perforation
    6. After abdominal surgery
    7. Diaphragmatic hernia
    8. Endoscopic variceal sclerosis
    9. After liver transplantation
  E. Heart diseases
    1. After coronary artery bypass graft surgery 
    2. Post–cardiac injury (Dressler's) syndrome
    3. Pericardial disease
  F. Obstetric and gynecologic diseases
    1. Ovarian hyperstimulation syndrome
    2. Fetal pleural effusion
    3. Postpartum pleural effusion
    4. Megis' syndrome
    5. Endometriosis
  G. Collagen vascular diseases
    1. Rheumatoid pleuritis
    2. Systemic lupus erythematosus
    3. Drug-induced lupus
    4. Immunoblastic lymphadenopathy
    5. Sj√∂gren's syndrome
    6. Familial Mediterranean fever
    7. Churg-Strauss syndrome
    8. Wegeners granulomatosis
  H. Drug-induced pleural disease
    1. Nitrofurantoin
    2. Dantrolene
    3. Methysergide
    4. Ergot alkaloids
    5. Amiodarone
    6. Interleukin-2
    7. Procarbazine
    8. Methotrexate
    9. Clozapine
  I. Miscellaneous diseases and conditions
     1. Asbestos exposure
     2. After lung transplantation
     3. After bone marrow transplantation
     4. Yellow nail syndrome
     5. Sarcoidosis
     6. Uremia
     7. Trapped lung
     8. Therapeutic radiation exposure
     9. Drowning
    10. Amyloidosis
    11. Milk of calcium pleural effusion
    12. Electrical burns
    13. Extramedullary hematopoiesis
    14. Rupture of mediastinal cyst
    15. Acute respiratory distress syndrome
    16. Whipple's disease
    17. Iatrogenic pleural effusions
  J. Hemothorax
  K. Chylothorax

63 - Transudative Pleural Effusion causes

   Transudative pleural effusions

  A. Congestive heart failure
  B. Cirrhosis
  C. Nephrotic syndrome
  D. Superior vena caval obstruction
  E. Fontan procedure
   F. Urinothorax
  G. Peritoneal dialysis
  H. Glomerulonephritis
   I. Myxedema
   J. Cerebrospinal fluid leaks to pleura
  K. Hypoalbuminemia
   L. Pulmonary emboli
  M. Sarcoidosis

Thursday, December 17, 2009

62 - Staging of Breast Cancer

TNM staging system for BREAST CANCER


Primary tumor (T) Definitions for classifying the primary tumor (T) are the same for clinical and for pathologic classification. If the measurement is made by physical examination, the examiner will use the major headings (T1, T2, or T3); if other measurements, such as mammographic or pathologic measurements, are used, the subsets of T1 can be used. Tumors should be measured to the nearest 0.1-cm increment. 
  TX
Primary tumor cannot be assessed
  T0
No evidence of primary tumor
  Tis
Carcinoma in situ
    Tis (DCIS)
Ductal carcinoma in situ
    Tis (LCIS)
Lobular carcinoma in situ
    Tis (Paget's)
Paget's disease of the nipple with no tumor (NOTE: Paget's disease associated with a tumor is classified according to the size of the tumor) 
  T1
Tumor less than or equal to 2 cm in greatest dimension
    T1mic
Microinvasion less than or equal to 0.1 cm or less in greatest dimension
    T1a
Tumor >0.1 cm but not >0.5 cm in greatest dimension
    T1b
Tumor >0.5 cm but not >1 cm in greatest dimension
    T1c
Tumor >1 cm but not >2 cm in greatest dimension
  T2
Tumor >2 cm but not >5 cm in greatest dimension
  T3
Tumor >5 cm in greatest dimension
  T4
Tumor of any size with direct extension to (a) chest wall or (b) skin, only as described below
  T4a
Extension to chest wall, not including pectoralis muscle
  T4b
Edema (including peau d'orange), or ulceration of the skin of the breast, or satellite skin nodules confined to the same breast
  T4c
Both T4a and T4b
  T4d
Inflammatory carcinoma
Regional lymph nodes—Clinical (N) 
  NX
Regional lymph nodes cannot be assessed (e.g., previously removed)
  N0
No regional lymph node metastasis
  N1
Metastasis to movable ipsilateral axillary lymph node(s)
  N2
Metastases in ipsilateral axillary lymph nodes fixed or matted, or in clinically apparenta ipsilateral internal mammary nodes in the absence of clinically evident axillary lymph node metastasis
 

    N2a
Metastasis in ipsilateral axillary lymph nodes fixed to one another (matted) or to other structures
  N3
Metastasis only in clinically apparenta ipsilateral internal mammary nodes and in the absence of clinically evident axillary lymph node metastasis; metastasis in ipsilateral infraclavicular lymph node(s) with or without axillary lymph node involvement, or in clinically apparenta ipsilateral internal mammary lymph node(s) and in the presence of clinically evident axillary lymph node metastasis; or metastasis in ipsilateral supraclavicular lymph node(s) with or without axillary or internal mammary lymph node involvement
 

  N3a
Metastasis in ipsilateral infraclavicular lymph node(s)
  N3b
Metastasis in ipsilateral internal mammary lymph nodes(s) and axillary lymph node(s)
  N3c
Metastasis in ipsilateral supraclavicular lymph node(s)
Regional lymph nodes—Pathologic (pN) 
  pNX
Regional lymph nodes cannot be assessed (e.g., previously removed, or not removed for pathologic study)
  pN0b
 

No regional lymph node metastasis histologically, no additional examination for isolated tumor cells [NOTE: Isolated tumor cells (ITC) are defined as single tumor cells or small cell clusters not >0.2 mm, which are usually detected only by immunohistochemical (IHC) or molecular methods but which may be verified on hematoxylin and eosin stains; ITCs do not usually show evidence of malignant activity (e.g., proliferation or stromal reaction)] 
    pN0(i–)
No regional lymph node metastasis histologically, negative IHC results
    pN0(i+)
No regional lymph node metastasis histologically, positive IHC results, no IHC cluster >0.2 mm
    pN0(mol–)
No regional lymph node metastasis histologically, negative molecular findings [reverse-transcriptase polymerase chain reaction (RT-PCR)]
    pN0(mol+)
No regional lymph node metastasis histologically, positive molecular findings (RT-PCR)
  pN1
Metastasis in 1 to 3 axillary lymph nodes, and/or in internal mammary nodes with microscopic disease detected by sentinel lymph nodes dissection, not clinically apparentc
 

    pN1mi
Micrometastasis (>0.2 mm, none >2.0 mm)
    pN1a
Metastasis in 1 to 3 axillary lymph nodes
    pN1b
Metastasis in internal mammary nodes with microscopic disease detected by sentinel lymph node dissection, not clinically apparentc
 

    pN1c
Metastasis in 1 to 3 axillary lymph nodes and in internal mammary lymph nodes with microscopic disease detected by sentinel lymph node dissection but not clinically apparentc (if associated with >3 positive axillary lymph nodes, the internal mammary nodes are classified as pN3b to reflect increased tumor burden)
 

  pN2
Metastasis in 4 to 9 axillary lymph nodes, or in clinically apparenta internal mammary lymph nodes in the absence of axillary lymph node metastasis
 

    pN2a
Metastasis in 4 to 9 axillary lymph nodes (at least one tumor deposit >2.0 mm)
    pN2b
Metastasis in clinically apparenta internal mammary lymph nodes in the absence of axillary lymph node metastasis
 

  pN3
Metastasis in greater than or equal to 10 axillary lymph nodes, or in infraclavicular lymph nodes, or in clinically apparenta ipsilateral internal mammary lymph nodes in the presence of 1 or more positive axillary lymph nodes; or in >3 axillary lymph nodes with clinically negative microscopic metastasis in internal mammary lymph nodes; or in ipsilateral supraclavicular lymph nodes
 

    pN3a
Metastasis in greater than or equal to 10 axillary lymph nodes (at lease one tumor deposit >2.0 mm), or metastasis to the infraclavicular lymph nodes
    pN3b
Metastasis in clinically apparenta ipsilateral internal mammary lymph nodes in the presence of greater than or equal to 1 positive axillary lymph nodes; or in >3 axillary lymph nodes and in internal mammary lymph nodes with microscopic disease detected by sentinel lymph node dissection, not clinically apparentc
 

    pN3c
Metastasis in ipsilateral supraclavicular lymph nodes
Distant metastasis (M) 
  MX
Distant metastasis cannot be assessed
  M0
No distant metastasis
  M1
Distant metastasis

aClinically apparent is defined as detected by imaging studies (excluding lymphoscintigraphy) or by clinical examination or grossly visible pathologically.
bClassification is based on axillary lymph node dissection with or without sentinel lymph node dissection. Classification based solely on sentinel lymph node dissection without subsequent axillary lymph node dissection is designated (sn) for "sentinel node" e.g., pN–(l+) (sn).
cNot clinically apparent is defined as not detected by imaging studies (excluding lymphoscintigraphy) or by clinical examination.



TNM Stage Groupings

Stage 0 
Tis
N0
M0
Stage I 
T1a
 

N0
M0
Stage IIA 
T0
N1
M0

T1 a  
N1
M0

T2
N0
M0
Stage IIB 
T2
N1
M0

T3
N0
M0
Stage IIIA 
T0
N2
M0

T1a
 

N2
M0

T2
N2
M0

T3
N1
M0

T3
N2
M0
Stage IIIB 
T4
N0
M0

T4
N1
M0

T4
N2
M0
Stage IIIC 
Any T
N3
M0
Stage IV 
Any T
Any N
M1

aT1 includes T1mic.





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