BIODATA

  Name: R.F
  Age: 30years
  Parity: P3ᶧ⁰
  LMP:10/03/17, LCB 3 Years ago
  Marital Status: Married
  Sex: Female
  Address: Soma, Religion: Islam, Tribe: Mandinka, Level of Education: Primary

PRESENTING COMPLAIN
  Feeling of movement in the abdomen
  Intermittent lower Abdominal Pain
   
HISTORY OF PRESENTING COMPLAIN
  She was apparently well until 5 months PTP When she started to experience feeling of movement in the abdomen and a sharp pain. She has a urine analysis and blood test done and was dx with gonorrhea on 2/03/2017. for which she was tx with flaggyl 2g, cipro 500mg, Doxy 100mg and Pcm 1g. On the 5/04/2017, pt. again presented with the same complain and USS was done on 30/3/2017 which showed a thick endometrium containing fluid measuring 15mm and presence of abundant free fluid in the douglas sac.The pt. took local herbs to help relieve the symptoms.

GYNAECOLOGICAL HISTORY

 Menarche was at 14years
 Menstruate for 5days in a regular cycle of 28days
 Associated with dysmenorrhea, but no clots, or intermenstrual bleeding.
 Changes 3 pads daily on 1st 3 days
 Coitarche was at 20years, no dysparenia, or post coital bleeding.
 She has no hx of vx infection
 Has hx of contraceptives which she started in 2015 (injectables which she received at a 3m interval) and    stopped use in May, 2016.
 Not aware of PAP smear and has not had one.

OBSTRETICS HISTORY
  P3ᶧ⁰, LCB: 2014
  1st pregnancy was in 2006, carried to term with no complications during or after pregnancy, delivered by SVD at Serrekunda Hospital leading to 3.0 kg a boy. The boy was breast fed for 1 year and 7 months, is 11 y/o, is healthy and is in school.


  2nd pregnancy was in 2013, carried to term with no complications during or after pregnancy, delivered by SVD at hospital in Soma leading to a girl. The girl was breast fed for 1 year and 4 months, is 4 y/o, and is healthy.
  3rd pregnancy was in 2014, carried to term with no complications during or after pregnancy, delivered by SVD at hospital in Soma leading to a girl. The girl was breast fed for 1 year and 7 months, is 3 y/o, and is healthy.

PAST MEDICAL HISTORY
  Not a known HTN, DM, Asthmatic, TB, SCD, Epilepsy, or any other chronic conditions.

PAST DRUG HISTORY
  Not on any herbal medication currently but was taking some 5 months PTP.
  No known food or drug allergy.

FAMILY AND SOCIAL HISTORY
  She is from a polygamous family, father had 2 wives, mum was the 2nd wife.
  No family history of hypertension, diabetes, TB, asthma or any other chronic condition.
  She is a housewife, she is the 1st out of 6 children. She does not smoke cigarette nor drink alcohol.


  Her husband is currently unemployed, smokes but have no hx of DM, HTN, asthma or TB as well as his      family and denies any hx of sexual infections.

Summary
  A 30 y/o multiparous woman, P3+0, LMP:10/03/17, LCB 3 years ago has presented with feeling of movement in the abdomen and intermittent sharp LAP urine analysis and blood test done and was dx with gonorrhea on 2/03/2017. for which she received appropriate treatment.                   

EXAMINATION
•       General examination - stable, not in any obvious distress, afebrile, not pale, anicteric and no signs of lymphadenopathy. No presence of kolechyia or edema. BP 130/90mmHg, PR 98bpm, R 19cpm

SYSTEMIC REVIEW
•       CNS: Headache, Dizziness
•       CVS: HS-S1 and S2 no mumurs
•       RESPIRATORY: NAD
•       GIT: NAD
•       REPRODUCTIVE: feeling of movement in the abdomen and intermittent sharp LAP
•       URINARY: Polyuria
  Abdomen: Full, MWR and umblicus is inverted. no scar or scarrification, female pattern hair distribution.

 ASSESSMENT: Endometriosis

PLAN: Cipro 500 mg BD 1/57
  Flaggyl 500 mg TDS 1/57
  PCM 1g TDS 1/57
  Appoitment 19-4-2017


Literature review
 
DEFINITION

Presence of functioning endometrium (glands and stroma) in sites other than uterine mucosa is called endometriosis. It is not a neoplastic condition, although malignant transformation is possible.
These ectopic endometrial tissues may be found in the myometrium when it is called endometriosis interna or adenomyosis. More commonly, however, these tissues are found at sites other than uterus and are called endometriosis externa or generally referred to as endometriosis.
Endometriosis is a disease of contrast. It is a benign but it is locally invasive, disseminates widely. Cyclic hormones stimulate growth but continuous hormones suppress it.



INCIDENCE
      Ten to fifteen percent of reproductive-aged women. 
      Occurs primarily in women in their 20s and 30s. Common in nulliparous woman. 
      Accounts for 20% of chronic pelvic pain. 
      One-third to one-half of women affected with infertility, have endometriosis. 

PATHOPHYSIOLOGY 

      The ectopic endometrial tissue is physiologically functional. It responds to hormones and goes through cyclic changes, such as menstrual bleeding. 
      The result of this ectopic tissue is “ectopic menses,” which causes bleeding, peritoneal inflammation, pain, fibrosis, and, eventually, adhesions. 

ENDOMETRIOSIS SITES
      Common
                        Ovary (bilaterally): 60%. 
                        Peritoneum over uterus. 
                        Anterior and posterior cul-de-sacs. 
                         Broad ligaments/fallopian tubes/round ligaments. 
                        Uterosacral ligaments. 
                        Bowel. 
                        Pelvic lymph nodes: 30%.

Less Common
      Rectosigmoid: 10–15%. 
      Cervix. 
Vagina. 
      Bladder. 
      Rare 
      Nasopharynx. 
 Lungs. 
      Central nervous system (CNS). 
      Abdominal wall. 
      Abdominal surgical scars or episiotomy scar. 
      Arms/legs.
      
      THEORIES OF ETIOLOGY
Though the mechanisms and etiology are unknown, there are four theories commonly cited. It is likely that multiple theories may explain the diverse nature of this disorder: 
a. Retrograde menstruation: Endometrial tissue fragments are retrogradely transported through the   fallopian tubes and implant there or intra- abdominally with a predilection for the ovaries and pelvic  peritoneum. 
b. Mesothelial (peritoneal) metaplasia: Under certain conditions, peritoneal tissue develops into    functional endometrial tissue, thus responding to hormones. 
c. Vascular/lymphatic transport: Endometrial tissue is transported via blood vessels and lymphatics. This can explain endometriosis in locations outside of the pelvis (i.e., lymph nodes, pleural cavity, kidneys). 
d. Altered immunity: There may be deficient or inadequate natural killer (NK) or cell-mediated response. This can explain why some women develop endometriosis, whereas others with similar characteristics do not. 
e. Iatrogenic dissemination: Endometrial glands and stroma can be im- planted during a procedure (e.g., C-section).

Endometriosis can be noted in the anterior abdominal wall. 

      GENETIC PREDISPOSITION 
      A woman with a first-degree relative affected with endometriosis has a 7% chance of being similarly
affected as compared with 1% in unrelated persons. With a positive family history, a patient may develop endometriosis at an earlier age than the family member. 

COMPLICATIONS OF ENDOMETRIOSIS
                           Endocrinopathy his may be mostly responsible for infertility 
                           Rupture of chocolate cyst 
                           Infection of chocolate cyst 
                           Obstructive features:
                –  Intestinal obstruction 
                        –   reteral obstruction hydroureter hydronephrosis renal infection 
                           Malignancy is rare, the commonest one being 
adenoacanthoma. 

      CLINICAL PRESENTATION
1.     Pelvic pain (that is especially worse during menses, but can be chronic): Secondary dysmenorrhea (pain begins up to 48 hrs. prior to menses). Dyspareunia (painful intercourse) as a result of implants on pouch of Douglas; occurs commonly, with deep penetration. Dyschezia (pain with defecation): Implants on rectosigmoid. 
2.     Infertility.
3.     Intermenstrual bleeding.
4.     Cyclic bowel or bladder symptoms (hematuria).
5.     Up to one-third of women may be asymptomatic.

SIGNS
1.     Fixed retroflexed uterus, with scarring posterior to uterus. 
2.     Tender uterus or presence of adnexal masses. 
3.     “Nodular” uterosacral ligaments or thickening and induration of utero- 
sacral ligaments. 
4.     Ovarian endometriomas: Tender, palpable, and freely mobile implanted   masses that occur within the ovarian capsule and bleed. This creates a small blood-filled cavity in the ovary, classically known as a “chocolate cyst.” 
5.     Blue/brown vaginal implants (rare).
The classic findings on physical exam are nodularities on the uterosacral ligament and a fixed retroverted uterus.

      DIAGNOSIS 
Clinical diagnosis is by the classic symptoms of progressively increasing secondary dysmenorrhea, dyspareunia and infertility. This is corroborated by the pelvic findings of nodules in the pouch of Douglas, nodular feel of the uterosacral ligaments, fixed retroverted uterus and unilateral or bilateral adnexal mass. However, physical examination has poor sensitivity and specificity. Many patients have no abnormal findings on examination.

Serum marker CA 125—A moderate elevation of serum CA 125 is noticed in patients with severe endometriosis. It is not specific for endometriosis, as it is significantly raised in epithelial ovarian carcinoma. However, it is helpful to assess the therapeutic response and in follow up of cases and to detect any recurrence after therapy.

Monocyte Chemotactic Protein (MCP-1) level is increased in the peritoneal fluid of women with endometriosis.

IMAGING
Ultrasonography is not much helpful to the diag nosis. TVS can detect ovarian endometriomas. Transvaginal (TVS) and Endorectal ultrasound are found better for rectosigmoid endometriosis. Magnetic Resonance Imaging (MRI) is a diag nostic tool. There is a characteristic hyperintensity on T1 weighted images and a hypointensity on T2 weighted images.
CT is better compared to ultrasonography in the diagnosis.

It is useful for deep infiltrating endo metriosis.
Colonoscopy, rectosigmoidoscopy and cystoscopy are done when respective organs are involved.
Laparoscopy is the gold standard. Confirmation is done by double puncture laparoscopy or by laparotomy.

Other benefits are: Confirmation of the lesion with site, size and extent. Biopsy can be taken at the same time. Staging (p. 309) can be done. Extent of adhesions could be recorded. Opportunity to do laparoscopic surgery if needed (p. 306) .

The classic lesion of pelvic endometriosis is described as ‘powder burns’ or ‘match stick’ spots on the peritoneum of the pouch of Douglas (see p. 309).

indings may be recorded on video or ( 2006) Microscopically some of these lesions contain endometrial glands, stroma and hemosiderin laden macrophages.

Biopsy confirmation of excised lesion is ideal but negative histology does not e clude it. one of the imaging techniques including ultrasound, can diagnose specifically the peritoneal endometriosis. Emperic medical treatment is usually not recommended except for pain relief and to reduce menstrual flow.

CLINICAL COURSE
·Thirty-five percent are asymptomatic. 
·Symptomatic patients may have increasing pain and possible bowel 
pain and possible bowel complications. 
·Often, there is improvement with pregnancy secondary to temporary  cessation of menses. 
·May be associated with infertility.

  TREATMENT
Medical (temporizing). The primary goal is to induce amenorrhea and cause regression of the endometriotic implants. 
All of these treatments suppress estrogen:
Gonadotropin-releasing hormone (GnRH) agonists (leuprolide): Suppress follicle-stimulating hormone (FSH); create a pseudomenopause. 
Depo-Provera (progesterone [+/– estrogen]): Creates a pseudopregnancy (amenorrhea). 
Danazol: An androgen derivative that suppresses FSH/luteinizing hormone (LH), thus also causing pseudomenopause. 
Oral contraceptives (OCPs): Used with mild disease/symptoms. 

Surgical 
Conservative (if reproductivity is to be preserved): Laparoscopic lysis and ablation of adhesions and implants. 
Definitive: Total abdominal hysterectomy and bilateral salpingo-oophorec- tomy (TAH/BSO). 
A GnRH agonist can be used in conjunction with surgical treatment. It is associated with osteoporosis and should be used for only six months. 

The pulsatile fashion of endogenous GnRH stimulates FSH secretion. GnRH agonists cause down regulation of pituitary receptors and suppress FSH secretion

General treatment issues
Patient participation in the decision-making process is essential as multiple options exist and endometriosis is potentially a chronic problem. Choosing which treatment to have will depend upon a number of factors. Summarizing how these factors influence decision making is difficult because each patient is different and the decisions are often complex. However, some general principles apply. For example, a woman in her late 40s with debilitating pain and severe disease who has completed her family can be offered a hysterectomy and bilateral salpingo-oophorectomy provided that all the endometriotic tissue is removed at the same time. On the other hand, a young nulliparous woman with a similar presentation will want as much normal tissue as possible conserved if she opts for surgery.

Conclusion  
The patient came to hospital complaining of feeling of movement in the abdomen and  intermittent lower abdominal pain for 5 months PTP.

She has a urine analysis and blood test done and was dx with gonorrhea on 2/03/2017 for which she was treated with flaggyl 2g, ciprofloxacin 500mg, Doxycycline 100mg and Paracetamole 1g. However, on the 5/04/2017, pt. again presented with the same complain and USS was done on 30/3/2017 which showed a thick endometrium containing fluid measuring 15mm and presence of abundant free fluid in the douglas sac.

Other positive finding was dysmenorrhea which is present in 70% cases. There is progressively increasing secondary dysmenorrhea. The pain starts a few days prior to menstruation; gets worsened during menstruation and takes time, even after cessation of period, to get relief of pain, (co menstrual dysmenorrhea). and usually begins after few years pain free menses. The site of pain is usually deep seated and on the back or rectum. 
Increased secretion of  PGF 2a, thromboxane B2 from endometriotic tissue is the cause of pain.

There were no other associated risk symptoms like abnormal menstruation, infertility, dyspareunia,  chronic pelvic pain, abdominal pain, etc in her case. Patient was prescribed Cipro 500 mg BD 1/57, Flaggyl 500 mg TDS 1/57, PCM 1g TDS 1/57 and given appoitment for 19-4-2017 for which she has not yet turned up.

References
1. Diamanti-Kandarakis, Evanthia; Dunaif, Andrea (December 2012). " Endometriosis Revisited: An Update on Mechanisms and Implications". Endocrine Reviews. 33 (6): 981–1030. doi:10.1210/er.2011-1034. PMID 23065822.
2. Endometriosis: First Aid for the Obstetrics and Gynecology, Third Edition by MATTHEW S. KAUFMAN, MD..
3. Endometriosis: Kaplan USMLE step 2 CK Obstetrics and Gynecology Lecture notes; 2014.
4.

Endometriosis: DC Dutta’s Textbook of Obstetrics 7E Revised edition; 2014.
5. Munir, Iqbal; Yen, Hui-Wen; Geller, David H.; Torbati, Donna; Bierden, Rebecca M.; Weitsman, Stacy R.; Agarwal, Sanjay K.; Magoffin, Denis A. (January 2004). "Insulin Augmentation of 17α-Hydroxylase Activity Is Mediated by Phosphatidyl Inositol 3-Kinase But Not Extracellular Signal-Regulated Kinase-1/2 . Endocrinology. 145 (1): 175–183. doi:10.1210/en.2003-0329.

 

 

 

 

 

 

 

 

 

 

 

 

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