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Friday, April 4, 2014

PAIN ORIGINATING IN THE ABDOMEN

1.     Partcial peritoneal inflammation
a.     Bacterial contamination,eg., perforated                       appendix. Pelvic inflammatory disease         
b.    ,eg ., perforated ulcer.pan creatitis,mittelschmerz
c.     Primary(spontaneous) peritonitis.this is acute orsubacute bacterial inflammation of the eritoneum.it occurs in patient with cirrhotic or malignant ascites,immune deficiency  states and in children with nephroticsyndromeor urinary tract infaction the commonest organismis Streptocccuus pneumoniae.
d.    Tuberculous peritonitis(seep.600).
e.     Chemical peritonitis develops when asterile but irritant fluide,e.g. bile,blood or pancreatic secretions,leaks into  the peritoneal cavity
f.      Granulomatous peritonitis can be caused by infections(berculosis,fungi,parasites), secondary adenocarcinoma,sarcoidosis,crohn's disease or foreign bodies(e.g.starch).
g.     Vasculties peritonitis occure when  there is gut  involvementin SLE,polyartiritis nodosa,systematic,sclerosis,dematomysities or Henoch-schonlein perpura.
h.    Familial Mediterranean fever is characterized  by recurrent episodes is acute  self –limiting  ser sitis especially involving the peritoneum(see p 1101).

2.     Mechanical obstruction of hollow viscrea                   
a.     Obstruction of the smallor large intense
b.    Obstruction of the biliary tree
c.     Obstructionof the ureter
3.     Vascular disrurbances
a.     Embolism orthrombosis
b.    Vasculer rupture
c.     Pressure or torsional occlusion
d.    Sickle cell anemia
4.     Abdomminal wall
a.Distortion or traction of mesentery
Vascular distrubance Afrequent misconception, despite abundant experience to the contrary pain associated with intraabdominal vascular disturbances is sudden and catasrrophic in nature the pain of embolism  of thrombosis of superior  mesenteric artery or that of impending rupture of an abdominal aortic aneurysm certainly may be severe and diffuse .yet.just as frequently ,the patient with occlussion of the superior mesenteric artery has only mild  continous diffuse pain for 2or3days before vascular collapse or finding of peritoneal inflammation appear.the early.seemingly  insignificant discomfort is caused by hyper istalsis rather than peritoneal inflammation .indeed ,absence of tenderness and rigidity  in the presence of continous ,defuse pain  in apatient likely to have vascular disease in quite charachteristic of occulision of superior mesenteric artery.abdominal pain with radiation to the sacralregion.flank or genetalia should always signal to the possible presence of a rupturing  abdominal aortoc aneurysm.this pain may persist over  operiod of several days before rupture and collapse occure.

Refered pain in abdominal disease     pain referredto the abdomen from the thorax , spin .or genitalia may prove avexing diagnostic problem.because diseases of upper part of abdominal cavity such as  acute cholecysitis or performated ulcer are frequently associated with intrathoracic  complication.Amost important ,yet often forgotten.dictum is that the possibility of intrathoracic disease must be consideredin every patient with abdominal pain,especially if the pain is  in the upper part of the abdomen.systematic questioning and examinationdirected toward directing myocardial or pulmonary infraction pneumonia.pericarditis or esophageal disease(the intrathooracic diseases that most often masquerade as abdominal emergencies)will of tenten provide sufficient clues to establish the poper diagnosis.Diaphragmaticpleuritis resulting from pneumonia or pulmonary infraction may cause pain in the right upper quadrant and pain in the supraclaicular area the latter radiation to be
pulposus.diabetes,or syphilis.it is nnot associated with food intake .abdominal destination .or changes in perspiration  Severe muscle  spam.as  in the gastric crises  of tabes dorsalis.is common but is either  relieved or is not accentuated by abdominal palpation .The pain is made worse by movement  of the spine and is usually confined to afew dermatomes. hyperesthesia is very common

The correct interpretation of acute abdominal pain is challenging since paper therapy may require urgent action .the unhurried approach suitable for the study of other condition is some times denied few other clinical situation demand greater gudgment because the most catastrophic of events may be for cast the subtlest of symptoms and signs.Ameticulously executed detailed history and phusical examination are of great importance .the etiologic classification in Table 13-1,although not complete,forms ausefull basis for the evaluation of patient s with  abdominal pain.
The diagnosis of "acure of surgical abdomen" is not aacceptable one because of its often mis leading and erroneous connotation.The most abvious of " acute abdomens"may not require operative intervention,and the mildest of abdominal pains may herald an urgently correctable lesion.any patient with abdominal pain of recent one set requires early and through evaluation and accurate diagnosis.

SOME MECHANISM OF PAIN ORIGINATING IN THE ABDOMEN…inflammation of partial peritoneum The pain of partial peritoneal inflammation is stead and aching in character and is located directly over the inflamed area,is exact referencebeing possible because it is transmitted somatic nerves suppling the peritoneal peritoneum.The intensivity of the pain dependent on the type and amount  of material towhich the periotoneal surfaces are exposed in agiven time period. The pain of peritoneal inflammation is invarariably  accentuated by pressure  or changes in  tension of peritoneum.whether produced by palpation or by movement .as in caughing or sneezing.the patient with peritonitis lies quietly in bed.preferring to avoid motion. In contrast to the patient with colic.who may writhe incessantly.
b.Trauma or infection of muscles

5.     Dustention of visceral surfaces,e.g.,hepatic or renal capsules
PAIN REFERRD FROM EXTRA ABDOMINAL SOURCE                                                                                                                                   
1.Thorax,e.g ., pneumonia, referred pain from coronary occlusion
2.Spin,eg   .,radiculitis from arthritis,herpes zoster
3.Genitalia,e.g.,torsion of the testicle

METABOLIC CAUSES

1.Exogenous
       a.Black widow spider bite
b.Lead poisoning and others      

2.Endogenous

a.    Uremia
b.     Diabetic ketoacidosis
c.      Porphyria
d.     Allergic factor(C'1 esterase inhibitor deficiency)

       NEUROGENIC CAUSES

1.Organic
       a. Tabes dorsalis

b.Herpes zoster
c.Casualgia and others

2. Functional
distinguished from the referred subscapular pain caused by acute disternation of the extrahepticbiliary tree.the ultimate decision as to the origin of abdominal pain may require deliberate and planned observation over  a period of several hours ,during which repeated questioning and examination  will provide the diagnosis  or suggest the appropriate studies.
Referred pain of thoracic origin is often accompanied by splinting of the involved hemithorax with respiratory lag and decrease in excursion more marked than that seen in the presence  of intraabdominal disease.in addition,apparent abdominal muscle spam caused by referred pain will diminish during the inspiratory  phase of respiration, where as it is persistent throughout both respiratory phase if it is of abdominal origin.palpation over the area of referred pain in abdomen also does not usually accentuated the pain and  in many instances actually seems to relieve it.

METABOLIC ABDOMINAL CRISES  pain of metabolic origin may simulate almost any other type of intraabdominal disease.Several mechanisms may be at work in certain instances, such as hyperlipidemia,the metabolic disease It self may accompanied by an intraabdominal pracess such as pan creatitis,which can lead to unnecessary laparatormy  unless recognized.C'1 esterase deficiency associated with angioneurotic edema is often associated  with episodes of severe abdominal pain.whennever the cause of abdominalpain is obsecure.ametabolic origin always must be considered.Abdominal pain is also the hallmark of familial Mediterrranean fever

NEUROGENIC CAUSES  Causalgic pain may occur in disease that injure  sensory nerves . it has aburning character and is usually limited to the distribution of given peripheral nerve.Normal stimuli such as touch  or change in temperature may be transformed into this type  of pain which is frequently present in a patient at rest

Pain arising from spinal nerves or roots comes and goes suddenly and is of lancinating type.it may caused by herped zoster,impingement by arthritis.tumors.heriiated nucleus

Hypoglycemia


·    Spontaneous hypoglycemia:
Develops in non diabetics.
Causes and investigations
Hypoglycemia in diapetics:

·       Hypoglycemic: blood glucose less than 3.5 ml mole/liter(63mg/dl)
·       Hypoglycemic coma: blood glugose less than 2.5 ml mole/dl                                  (45mg/dl)                  

·       Occures in those on insulin therapy.
·       Rare in those on sulphonylurea.
·       Very rare in those on metformin.

Ø Common symptoms of hypoglycemia:

Ø Clinical features of hypoglycemia:

Ø Causes of hypoglycemia:

Ø Risk factors for severe hypoglycemia:
Ø

Marbidity of severe hypoglycemia in diabetic pationts:


Ø Prevention of hypoglycemia:

Ø Management of hypoglycemia:

Davdson page (823-826).
Davdson 20th edition.



Defferential diagnosis:

·       Cardigenic shock       (1)
·       Hypoglycemia           (2)
·       Myxoeodema coma  (3)

Report on:                          
·       level of consciousness.
·       Skin temp .- Sweat.
·       Pulse rate and volume.
·       Blood pressure.





Hyposplenism

         Absent or reduced splenic function, usually due to surgical removal, congenital aplasia, tumor replacement, or splenic vascular accident.
         Red blood cell abnormalities, including the presence of inclusions, nucleated red blood cells and target cells are commonly present. Persistent thrombocytosis with increased risk of thrombosis. Patients with hyposplenism are at increased risk of bacterial sepsis, especially due to infection by Pneumococci.
Conditions associated with hyposplenism:
1-    Sickle cell anemia
2-    Gluten induced enteropathy (Coeliac disease).
3-    Crohin's Disease and Ulcerative colitis
4-    Myelofibrosis and essential thrombocytosis
5-    SLE and RA
6-    Lymphoma and Multiple Myeloma
7-    Splenic irradiation and emolization
Diagnosis:
Determined by anatomic presence or absence of the organ, its size, and any lesions.
Function can be assessed by
Radiologic Techniques: X-ray, ultrasound, tomography, MRI, radionucleotide scanning
Morphologically: Peripheral blood smear- presence of Howell-Jolly bodies.
Complications:
Lifelong risk for Overwhelming Postsplenectomy infection (OPSI) Caused by Streptococcus pneumoniae and gram negative bacteria
Initial Symptoms: fever, chills, muscle aches, headache, vomiting, diarrhea, and abdominal pain
Progressive symptoms: bacteremic septic shock, extremity gangrene, convulsions, and coma
Mortality rate of 50-80% from onset of initial symptoms, 68% of those deaths occur within 24 hours and 80% occur within 48 hours
Prevention: routine vaccinations and prophylactic antibiotics.




Hypersplenism

Hypersplenism is a type of disorder which causes the spleen to rapidly and prematurely destroy blood cells.
Causes:
   It may be caused by a variety of disorders. Sometimes, it is brought on by a problem    
   within the spleen itself and is referred to as primary hypersplenism.
   Secondary hypersplenism results from another disease such as Malaria, RA, TB, or
   polycythemia vera .
Clinical presentation of hypersplenism include:
       * Splenomegaly
       * Easy bruising, epistaxix, hematemesis or hematuria
       * Manifestations of anemia
       * Fever and recurrent infections
       * Manifestations of the cause of splenomegaly
Diagnosis of hypersplenism begins with review of symptoms and patient history, and careful palpation of the spleen.
Blood counts indicate decreases in white blood cells, red blood cells, or platelets.
Bone marrow examination showed normocellular or hpercellular marrow.
Treatment
         In secondary hypersplenism, the underlying disease must be treated to prevent further sequestration or destruction of blood cells,
         In severe cases, the spleen must be removed. Splenectomy will correct the effects of low blood cell concentrations in the blood.
Prognosis
   Depends on the underlying cause and progression of the disease. Left untreated, spleen enlargement can lead to serious complications. Hypersplenism can also lead to complications due to decreased blood cell counts.



Prevention
   Some of the underlying causes of hypersplenism or enlarged spleen can be prevented, such as certain forms of anemia and cirrhosis of the liver. In other cases, the hypersplenism may not be preventable.


Splenomegaly. Functions of the spleen:

 Functions of the spleen:
1-       Filters out and destroys old and damaged blood cells,  
     intraerythrocyte inclusions and foreign particles.
2-       Plays a key role in preventing infection by producing lymphocytes and acting as a first line of defense against invading pathogens.
     3- Stores RBCs and platelets.
     4- Hematopoietic Function
Causes of Splenomegaly:
             Infection        
                            Viral: EBV, CMV, HIV and Hepatitis.
                             Bacterial: Salmonella, Brucella,  SBE, TB and Syphilis.
                            Protozoal: Malaria, Toxoplasma and  leishmania.
                            Fungal: Histoplasmosis and Coccidiodmycosis
              Red blood cell destruction   
                                    Spherocytosis , Thalassemia , G6PD, PKD and AIHA
             Venous outflow obstruction    
                                   Cirrhosis , portal hypertension  and  splenic vein thrombosis
             Immune Response:
                                  SLE, RA and Felty’s Syndrome
            Infiltrative :
                                 Sarcoidosis,  Amyloidosis and Gaucher disease
            Neoplastic                          
                                  Lymphoproliferative  (HD, NHL CLL)
                                   Myeloproliferative    (CML, PCV, ETT, MF)
                                   Hairy Cell Leukemia, ALL and  AML
                                   Sarcoma and Metastatic carcinoma
             Miscellaneous :

                                  Trauma, splenic cysts and hemangioma


Lymphadenopathy

Introduction:    
          Infrequently, patients will note enlarged lymph nodes and present with the chief complaint of having a nodule, a swollen gland, a "knot," or enlarged lymph nodes. More commonly, patients do not recognize that they have significantly enlarged lymph nodes, and the physician discovers the lymphadenopathy. Since lymphadenopathy can be associated with a wide range of disorders spanning relatively benign medical problems such as streptococcal pharyngitis to life-threatening malignancies, the discovery of enlarged nodes represents an important physical finding that demands a systematic evaluation.
          In searching for lymph nodes, one must be gentle; otherwise, lymph nodes that are only minimally enlarged or embedded in tissue may not be apparent. Particular attention should be directed to the size, shape, and consistency of enlarged nodes. Lymph nodes that are smooth and relatively soft, but slightly enlarged, may be normal and reveal only hyperplasia when biopsied. Enlarged lymph nodes that have an irregular shape and a rubbery, hard consistency may be infiltrated by malignant cells. Tender nodes are suggestive of an inflammatory process. Matted nodes or nodes fixed to underlying structures should raise the question of malignancy or infection; freely movable nodes are more likely to occur in benign conditions.
          The enlargement of lymph nodes, either localized or generalized, can be the consequence of several different pathologic mechanisms. Lymphadenopathy may represent an increase in the number and size of lymphoid follicles with proliferation of lymphocytes as a response to a new antigen. There can be enlargement of lymph nodes with infiltration of the node by cells normally not present, such as metastatic tumor or leukemic cells. Lymphadenopathy can occur secondary to unknown stimuli that cause normal cells to become transformed to lymphoma cells and to proliferate autonomously. Lymph nodes can be infiltrated by polymorphonuclear cells, a condition called lymphadenitis, or lymph nodes can be infiltrated by macrophages laden with metabolites, as in lipid storage diseases.

Possible causes of lymphadenopathy
I.                  Generalized lymphadenopathy
Generalized lymphadenopathy is defined as enlargement of more than 2 noncontiguous lymph node groups.
A.   Infections
1.     Viral
§  Common upper respiratory infections
§  Infectious mononucleosis
§  Cytomegalovirus (CMV) infection.
§  Human immunodeficiency virus (HIV).
§  Rubella
§  Varicella
§  Measles
2.     Bacterial
§  Septicemia
§  Typhoid fever
§  Tuberculosis
§  Syphilis
§  Plague
3.     Protozoal as Toxoplasmosis.
4.     Fungal as Coccidioidomycosis.
B.   Autoimmune disorders and hypersensitivity states
1.     Juvenile rheumatoid arthritis
2.     Systemic lupus erythematosus
3.     Drug reactions (eg, phenytoin, allopurinol and INH)
4.     Serum sickness
C.   Storage Diseases
1.     Gaucher disease
2.     Niemann-Pick disease.
D.   Neoplastic and proliferative disorders
1.     Acute leukemias (ALL, AML)
2.     Lymphomas (Hodgkin, non-Hodgkin)
3.     Neuroblastoma
4.     Histiocytoses.


II. Regional lymphadenopathy
A.   Cervical
                                                                                     i.      Viral upper respiratory infection
                                                                                   ii.      Infectious mononucleosis
                                                                                iii.      Rubella ……
                                                                                iv.      Catscratch disease
                                                                                   v.      Streptococcal pharyngitis
                                                                                vi.      Acute bacterial lymphadenitis
                                                                              vii.      Toxoplasmosis
                                                                           viii.      Tuberculosis/atypical mycobacterial infection
                                                                                ix.      Acute leukemia
                                                                                   x.      Lymphoma
                                                                                xi.      Neuroblastoma
                                                                              xii.      Rhabdomyosarcoma
                                                                           xiii.      Kawasaki disease.
                                                                           xiv.      Oral and dental infections
                                                                              xv.      Acute lymphadenitis
B.   Occipital
                                                                                     i.      Pediculosis capitis
                                                                                   ii.      Tinea capitis
                                                                                iii.      Secondary to local skin infection
                                                                                iv.      Rubella
C.   Preauricular
                                                                                     i.      Local skin infection
                                                                                   ii.      Chronic ophthalmic infection
                                                                                iii.      Catscratch disease
D.   Mediastinal
                                                                                     i.      Acute lymphoblastic leukemia
                                                                                   ii.      Lymphoma
                                                                                iii.      Sarcoidosis
                                                                                iv.      Cystic fibrosis
                                                                                   v.      Tuberculosis
                                                                                vi.      Histoplasmosis
                                                                              vii.      Coccidioidomycosis
E.   Supraclavicular
                                                                                     i.      Lymphoma
                                                                                   ii.      Tuberculosis
                                                                                iii.      Histoplasmosis
                                                                                iv.      Coccidioidomycosis
F.    Axillary
                                                                                     i.      Local infection
                                                                                   ii.      Catscratch disease
                                                                                iii.      Brucellosis
                                                                                iv.      Reactions to immunizations
                                                                                   v.      Lymphoma
                                                                                vi.      Juvenile rheumatoid arthritis
G.  Abdominal
                                                                                     i.      Acute mesenteric adenitis
                                                                                   ii.      Lymphoma
H.  Inguinal bacterial infections 
                                                                                     i.      Local infection    Diaper dermatitis
                                                                                   ii.      Insect bites
                                                                                iii.      Syphilis                Lymphogranuloma venereum

          In most patients with lymphadenopathy, a diagnosis can be made after a careful history, physical examination, and appropriate testing including hematologic parameters, serologic tests, skin tests, and routine x-rays. If a specific diagnosis cannot be established after appropriate evaluation, but infection is suspected, cautious observation after appropriate cultures have been obtained may be warranted. On the other hand, if the diagnosis cannot be established and a malignancy is a major concern, biopsy of a lymph node is appropriate.

          Although the differential diagnosis of lymphadenopathy may be broad and sometimes initially confusing, the careful gathering of data from the history, physical examination, and appropriate laboratory tests will resolve the differential in the vast majority of patients.