Name of Student: TOCAO, XYLIA SAHARA E. Date of ER duty :December 3-4, 2013

Patient Data

Hospital:SPMC Case number: 2569775Date of Admission: December 3, 2013 Room number: surgery eastTime of Admission :10:45 AM

Admission under the service/s of: Dr. WongType of Admission (Stat/ Elective):ElectiveType of core competency: III ( Esophagus,Duodenum,& Small intestines )Source of History data & Reliability: Patient , 95%

HISTORY:

General Patient Data

This is a case of Susan Del Ayre , a 39 year old male, married from Mineral village,Davao city, who came in due to abdominal pain Chief complaint: abdominal pain History of Present illness:

1 month prior to admission , the patient underwent an EXLAP operation at Mati city for ectopic pregnancy.

3 weeks prior to admission, the patient had diffuse abdominal pain with pain scale of 5 over 10 .No consultation and no medications taken.

1 week prior to admission, the patient noticed change in the bowel habits .She opted for consultation in this institution and was advised for admission.

Past Medical History:

The patient is not hypertensive, non diabetic , non asthmatic .

She underwent EXLAP operation at Mati city for ectopic pregnancy

Family History:

There are no other heredofamilial diseases like hypertension, diabetes mellitus , bronchial asthma and cancer reported.

Personal/Social History:

She is a non smoker but an occasional alcoholic beverage drinker . She has no allergies to food and drugs .

GYNECOLOGIC HISTORYPatient had her menarche at 12 years old. Subsequent menstrual periods were

regular lasting for 7 days moderate in quantity associated with occasional dysmenorrhea She had her sexual debut at 19 years old with 1 sexual partner who eventually became her husband.

OBSTETRIC HISTORY

The patient is multigravida G2P1 (2011). Her last menstrual period was last November 25, 2012. She claimed to have urinary tract infection during her first pregnancy and treated with unrecalled antibiotics. Her first pregnancy was delivered via normal spontaneous vaginal delivery ,full term,female. She had an ectopic pregnancy and underwent EXLAP operation last November 2013.

Review of Systems:

General: no recent weight loss,body weaknessEyes: no redness, no unusual dischargeEar: no pain, tinnitus Nose: no history of sinusitis , obstructionMouth: no gum bleeding, tonsillitisPulmonary: no difficulty of breathing, cough, hemoptysis and hematemesisCardiovascular: non hypertensive, (-)palpitationGastrointestinal: no change in bowel habits like constipation and diarrhea, no history of peptic ulcer , pain and food intoleranceGenitourinary:no history of stones, dysuria, hematuriaMusculoskeletal: no history of body weaknessNeurologic: no history of seizures, head trauma

Physical Examination:

GENERAL:

awake, not in respiratory distress.

VITAL SIGNS:

temperature:36.3 oC blood pressure: 120/80 mmHgpulse rate: 96 bpm respiratory rate: 22 cpm

SKIN:Inspection : no rash, (-) abrasions left arm Palpation: good skin turgor, dry skin

HEAD:Inspection: normocephalic, no lice & nits notedPalpation: (-) mass

EYES:Inspection: anicteric sclerae, pinkish palpebral conjunctivae

EARS:Inspection: non erythematous, no cerumen notedPalpation: mobile,firm, non tender

NOSE:Inspection: nasal septum in midline positionPalpation: no sinus tenderness

THROAT:Inspection: no tonsillar enlargement, non erythematous

NECK:Inspection: no thyromegalyPalpation: (-) cervical lymphadenopathy

CHEST/LUNGS:Inspection: (-) use of accessory muscles for breathingPalpation: (-) tendernessPercussion: dullness lower lung fieldAuscultation: harsh breath sounds

HEART:Inspection:adynamic precordiumPalpation: no thrills /heavesAuscultation: good S1 and S2, no murmurs noted

ABDOMEN:Inspection:flabbyAuscultation: normoactive bowel sounds at 10 per minutePercussion: tympaniticPalpation: (+) tenderness

EXTREMITIESINSPECTION:full range of motion Palpation: full pulses, CRT <2 seconds

NEUROLOGIC EXAM:

GCS: 15Eye opening: 4Verbal response:5Motor:6

awake, conscious, oriented to person , place and time.

CRANIAL NERVES:

I not assessedII isocoricIII, IV,VI pupils equally round and reactive to light and accommodationV (+) corneal reflex, able to distinguish sharp and blunt stimuli VII able to perform facial expressions like smiling and frowningVIII able to hear soft and loud spoken wordsIX (+) gag reflexX (-) difficulty of swallowingXI able to raise shoulders against resistanceXII able to protrude tongue and move it up, down and side

MOTOR:

R 5/5 5/5 L

5/5 4/5

REFLEX:

R ++ ++ L

++ ++

SENSORY:

R 100% 100% L 100% 100%

IMPRESSION:Partial intestinal obstruction probably secondary to post op adhesion , S/P EXLAP for ectopic pregnancy , November 2013, Mati

CASE DISCUSSION:

This is a case of SD , a 39 year old male from Mineral village, Davao city who came in due to abdominal pain.

For the history of present illness, 1 month prior to admission , the patient underwent an EXLAP operation at Mati city for ectopic pregnancy.

3 weeks prior to admission, the patient had diffuse abdominal pain with pain scale of 5 over 10 .No consultation and no medications taken.

1 week prior to admission, the patient noticed change in the bowel habits .She opted for consultation in this institution and was advised for admission

Intestinal obstruction is a partial or complete blockage of the bowel that prevents the contents of the intestine from passing through.

Postoperative intraperitoneal adhesions, or bands, resulting from any type of abdominal surgery, are the main cause of adhesive postoperative small bowel obstructions, which represent a life-long issue. Recurrences after operated adhesive postoperative SBO are a threatening potentiality for patients and a difficult problem facing any surgeon.

Adhesions are nonanatomic connections of fibrous tissue between normal peritoneal surfaces. Postoperatively, they have been classified as de novo or reformed ( Table 1 ).[1] De novo, or type 1, adhesions are adhesions that develop (i.e., are newly formed) at sites that did not have adhesions at an initial surgical procedure. In contrast, re-formed, or type 2, adhesions are classified as adhesions that develop at the sites of previous adhesiolysis. Types 1 and 2 are further classified into A and B subgroups. Subgroup A adhesions are seen at the sites where no operative procedure was performed (type 1A) excluding prior adhesiolysis (type 2A). In contrast, subgroup B adhesions develop at the sites that underwent surgical procedures without adhesiolysis (type 1B; e.g., myomectomy, ovarian cystectomy, etc.) or in addition to adhesiolysis (type 2B).

Adhesions develop after an injury to the normal peritoneal tissue. This injury can result from surgery,

trauma, inflammation, infection, or foreign body placement in the peritoneal cavity. After injury to the

normal mesothelial cells overlaying the peritoneal surface, the healing process starts. Vasoactive

substances such as histamines and kinins are released by the disruption of stromal mast cells

increasing vascular permeability, which contributes to the collection of a fibrin-rich exudate that covers

the injured area. Two processes occur essentially simultaneously. In one, the fibrin polymers in this

exudate interact with fibronectin to form the fibrin gel matrix, which consequently produces fibrin bands

between the injured areas. At the same time, fibrinolysis starts. Fibrinolysis dominates at sites where

healing occurs without adhesions. In contrast, if fibrinolysis is impaired, this imbalance may result in the

persistence of the fibrinous mass. Subsequently, proliferating fibroblasts invade this area and deposit

extracellular matrix material including collagen that contributes to the formation of adhesion. After

elicitation of angiogenesis factors such as vascular endothelial growth factor (VEGF), proliferation of

endothelial cells initiates the development of vascular structure within the adhesion tissue. Thus,

different mechanistic steps, some of which have been described above, regulate the healing process,

with imbalances in any of these potentially contributing to adhesion development. Furthermore, it is

likely that these activities are more pronounced at sites with prior fibrosis, such as those undergoing

adhesiolysis.

Ischemia has been proposed as the most important insult that leads to adhesion development. [2] It has

been demonstrated that fibroblasts in the adhesion tissues have different phenotype (myofibroblasts)

than do the normal peritoneal tissue fibroblasts. More importantly, it has been shown that conversion of

these cells from the normal phenotype to the adhesion phenotype can be induced by hypoxia. [2] The

adhesion phenotype has been thoroughly characterized at the molecular level.[2] Compared with

peritoneal fibroblasts, adhesion fibroblasts have a significant increase in the basal mRNA levels for

collagen I, fibronectin, matrix metalloproteinase-1 (MMP-1), tissue inhibitor of metalloproteinase-1

(TIMP-1), transforming growth factor (TGF)-β1, (TGF)-β1, cyclooxygenase-2 (COX-2), and interleukin

(IL)-10. Also, adhesion fibroblasts manifested lower apoptosis rate and higher protein nitration

compared with that of normal peritoneal fibroblasts.

Tissue plasminogen activator (tPA) and plasminogen activator inhibitor type-1 (PAI-1) are intracellular

enzymes found in the peritoneal mesenchymal cells. These constitute the intrinsic protective fibrinolytic

activity of fibroblasts. In fact, the ratio between these enzymes can be considered as a better marker of

fibrinolytic potential than just using tPA or PAI-1 levels individually. The tPA/PAI-1 ratio has been shown

to be 80% higher in normal peritoneal fibroblasts than in adhesion fibroblasts. Under hypoxic conditions,

this ratio significantly decreases in normal fibroblasts (90%), with an even more exaggerated decrease

observed in adhesion fibroblasts (98%).

MMPs and TIMPs are crucial proteolytic enzymes in the extracellular matrix remodeling process of

healing. Similarly, any imbalance in these systems may contribute to tissue fibrosis and adhesion

development. Hypoxia has been shown to inhibit MMP-1 and MMP-9 and augment TIMP-1

expression.This decrease in the MMP:TIMP ratio during hypoxia (98%) may favor the increase in

extracellular matrix production and the decrease in turnover and degradation that eventually may lead to

tissue fibrosis and adhesion development.

COX-2 enzyme has been shown to have an important role in the regulation of inflammatory and

angiogenesis steps of postoperative adhesions development. In adhesion fibroblasts, the expression of

COX-2 is significantly increased compared with that of the normal fibroblasts. Hypoxia enhances the

level of COX-2 expression in normal fibroblasts whereas there is no change in adhesion fibroblasts. It

has been reported that the normal fibroblasts acquire adhesion phenotype after transfection with COX-2

sense adenovirus. Furthermore, COX-2 antisense adenovirus transfection decreases the adhesion

phenotype characteristics in adhesion fibroblasts. COX-2 inhibitors, such as celecoxib, tenoxicam, and

pentoxifylline, have been reported to reduce postoperative adhesions through their anti-angiogenic, anti-

inflammatory, and antioxidant effects in animal studies.

The surface expression of certain adhesion and costimulatory molecules on peritoneal fibroblasts differs

among adhesion tissue and normal peritoneum. We have shown that elimination of adhesion fibroblasts

by allogeneic lymphokine-activated killer (LAK) cells is more pronounced than is the effect of LAK cells

on normal peritoneal fibroblasts. This enhanced killing has also been shown in the hypoxia-treated

normal peritoneal fibroblasts, supporting a contributory role of hypoxia in the adhesion phenotype

development. Furthermore, a deficient, suppressed, or overwhelmed natural immune system has been

proposed as an underlying mechanism in adhesion development