Cryptic Pregnancy

Cryptic Pregnancy
Cryptic pregnancy is a condition whereby a pregnant woman is unaware of her pregnancy until labor. During this pregnancy there is little or no detectable Human chorionic Gonadotropin (hCG) in the mothers system.

Cryptic Pregnancy (Picture Credit; parents24.)

Very often, bodily symptoms of pregnancy (nausea, amenorrhea and abdomen swelling) are absent or greatly reduced, and neonates tend to be underweight; in many cases, pregnancy goes undetected also by relatives and physicians.

Cryptic pregnancy differs from to denial of pregnancy, a psychological condition, where the woman is subconsciously aware of her pregnancy, but denies its existence.

Some of these women do not know that they are indeed pregnant and some of them do know, but the medical community refuses to recognize that these pregnancies exist.

 It is estimated that about 1 in 450 pregnant women doesn't know her pregnancy status until 20 weeks/ 5months or later (more than halfway through the pregnancy), and 1 in 2,500 is unaware of her pregnancy until she actually goes into labor.


Causes

This can be medical, social or both
Medical;

• Hormonal imbalance as seen in:

           -Poly Cystic Ovarian Syndrome (PCOS).
           -Peri-menopause, which can begin as early as age 30, and go undetected.
           -Recently pregnant women whose hormones have not gone back to normal before getting pregnant again.
           -Lactating mothers whose hormones are not back to normal, before getting pregnant again.
           -Women with a very low body fat percentage, causing a hormonal imbalance, like in female athletes.
           -Women who have recently used or are currently using a birth control method such as the "Norplant", "Deprovera" Injection or the "Mirena Coil", that continually releases hormones into the body.

• Anterior Placenta; If the placenta is positioned at the front of the uterus (an anterior placenta), the baby’s movements may not be felt as plainly.

Social
    Ignorance: while most women understand that pregnancy means their periods will (probably) stop and that their bodies will change shape, not all women are well-informed enough to notice subtler signs such as breast tenderness, constipation, etc. If the woman does not gain much weight and she continues to bleed while pregnant, she may not realize she is pregnant.
    Believe: when a woman truly believes she cannot become pregnant (e.g due to her use of an IUD, or due to many years of trying without success), she can fail to correctly interpret fetal movement, and can convince herself it is just indigestion or gas.  

Signs and Symptoms Each woman has a different experience with cryptic pregnancy.

Here there may be Typical symptoms of pregnancy such as:
-Nausea/vomiting
-Fatigue
-Frequent urination
-Food aversion
-Increased appetite
-Weight gain
-Heart burn
-Back pain
-Metallic taste in mouth
-Abdominal cramping/round ligament pain
-Headaches

Atypical Symptoms such as;
-Negative urine and blood pregnancy tests
-Continued periods
-Weight loss (though this can also occur in a "standard" pregnancy)
-The pregnancy symptoms may come and go. You may not "feel" pregnant all the time. Oftentimes during the menstruation, the pregnancy symptoms will subside. As soon as the menstruation is over, the symptoms will begin again. This is a VERY strong sign of a cryptic pregnancy, especially during the first few months. 
-Early labor signs that occur off and on for weeks or even months (not preterm labor)
-An extended gestational period / pregnancy, typically of 17 months or longer   
-Slow growth of the abdomen/pregnant belly

Complications Of Cryptic Pregnancy
    -The possibility of birth defects
    -Blood type incompatibility between you and your baby
    -Hypertension
    -Preeclampsia
    -High Blood Pressure

Important Points To Note;

• In Cryptic pregnancy, ultrasound is mostly negative; showing the Uterus as normal and empty

• None of these babies have been born before 17 months and some have gone as long as 3 or 4 years. 
• Multiples are common with cryptic pregnancies
• The labor in these pregnancies are normally prodromal. This means the patient could be in labor off and on for weeks, even months. 

Diagnosis
 The use of Doppler which reads the baby's heartbeat to be at least 110 to 160 and a  Finger pulse which reads the patients heartbeat to be 80 or less,

Differential Diagnosis

• Ovarian cysts, 
• Fibroids,
• UTIs (urinary tract infection),
• PCOS (polycystic ovarian syndrome),  
• pre-mature menopause,  
• menopause,
• peri-menopause,
• phantom pregnancy

Periodic symptoms of Labor in cryptic pregnancyinclude;
Back pain- low or high
Nausea/vomiting
Headaches
Dizziness
Chills
Hot flashes
Cold sweats
Vision issues
Diarrhea
generalized body pain
pain radiating from the hips down to the legs
Sudden episodes of nausea followed by sudden intense hunger
Sudden urges to urinate;  incontinence to some extent
Palpitations
Heart burn
Over all tension and tightness in the entire torso
Metallic taste in mouth
Period type cramps- can become very intense
The entire vaginal area can ache and feel bruised
Swelling of vaginal walls- this happened because of increased blood flow to the area and can make the vagina feel tight and shorter
sharp shooting pains in the breast
Extreme thirst
Severe irritability
Sudden severe mood swings
Extreme fatigue
Severe constipation
Episodes of sudden energy or feeling uneasy
Strong Braxton Hicks contractions
Stabbing pains in the sides
Sharp pains, dull aches, pinches, tugs, pulls etc anywhere in the abdomen.
Cervical aches, pinches, burning and sharp pains that may feel like being stabbed with a needle

Some or all of this may be felt and it occurs intermittently. Some patients wake up in the middle of the night and suddenly have to push.

Once a diagnosis has been made, inform and counsel the patient.

(Picture Credit; amazing pregnancy pictures)

      




NOTES;

1  Cryptic Pregnancy Support Group |

2  Del Giudice, M. "The evolutionary biology of cryptic pregnancy: A re-appraisal of the "denied pregnancy" phenomenon.". Med Hypotheses. Retrieved 13 April 2013.

3  Jena, Pincot (8 November 2011). "How Can You Be Pregnant (For Months) And Not Know It?". Huffington Post. Retrieved 13 April 2013

4  Wikipedia | Cryptic pregnancy website

Fibrodysplasia Ossificans Progressiva (FOP) Or Stone Man Syndrome

Fibrodysplasia Ossificans Progressiva (FOP) Or Stone Man Syndrome


FOP is a disorder in which muscle tissue and connective tissue (tendons and ligaments) are gradually replaced by bone (ossified), forming bone outside the skeleton (extra-skeletal or heterotopic bone) that constrains movement.

It is a rare idiopathic or autosomal dominant condition of irregular penetration and pre-pubertal onset, in which connective/interstitial tissues undergo extensive fibrosis and heterotopic ossification of ligaments, tendons, muscle, fascia, aponeuroses and skin, first seen in late childhood as firm masses. The abnormal development of bone may lead to stiffness in affected areas and may also limit movement in affected joints, e.g., knees, wrists, shoulders, spine, and/or neck. It can also be called Myositis ossificans progressiva.

 Fibrodysplasia Ossificans Progressiva (Pictures Credit; reddit)

First described in 1736 by John Freke (1688–1756), an English surgeon who was instrumental in separating the profession of Surgeons from that of Barbers.

It affects about 1 in 2 million people, has no gender, ethnic, racial or geographic predilection. About 800 confirmed cases have been documented across the globe.

In Stone Man Syndrome, there is mutation of a gene in the bone morphogenetic protein (BMP) pathway, which is important during the formation of the skeleton in the embryo and the repair of the skeleton following birth.
A mutation in the gene ACVR1 (also known as activin-like kinase 2 [ALK-2]) is responsible for the disease. ACVR1 encodes activin receptor type-1, a BMP type-1 receptor.
It is believed that this mutation in ACVR1 gene may change the shape of the receptor under certain conditions and disrupt mechanisms that control the receptor's activity.

As a result, the receptor may be constantly turned on (constitutive activation). Constitutive activation of the receptor causes overgrowth of bone and cartilage and fusion of joints, resulting in the signs and symptoms of fibrodysplasia ossificans progressiva.


Risk Factors
Often precipitated by soft tissue injury or Minor trauma e.g;
  intramuscular injections,
  mandibular blocks for dental work,
  muscular stretching,
  muscle fatigue,
  blunt muscle trauma from bumps,
  bruises,
  falls
  influenza-like viral illnesses

Signs and Symptoms
    The hallmark symptom of fibrodysplasia ossificans progressiva (FOP) is a congenital malformation of a newborn's big toe. This malformations of the great toe, which is apparent at birth, presents as hallux valgus, malformed first metatarsal, and/or monophalangism.
   During the first decade of life, sporadic episodes of painful soft tissue swellings (flare-ups) occur. Though some exacerbations spontaneously regress, Episodic soft tissue injuries may lead to stiffness in affected areas, limited movement, and eventual ankylosis of affected joints (neck, shoulders, elbows, hips knees, wrists, ankles, jaw, often in that order).

    Heterotopic ossification is typically seen first in the dorsal, axial, cranial, and proximal regions of the body and later in the ventral, appendicular, caudal, and distal regions. Although the cervical spine often becomes ankylosed early in life, any minimal residual movement may eventually result in painful arthritic symptoms.

    Other skeletal anomalies commonly associated with fibrodysplasia ossificans progressiva include; short malformed thumbs, clinodactyly, short broad femoral necks, and proximal medial tibial osteochondromas. Several skeletal muscles, including the diaphragm, tongue, and extraocular muscles, are spared from fibrodysplasia ossificans progressiva. Cardiac muscle and smooth muscle are also spared from heterotopic ossification.

   The Classic Defining features of  Typical stone man syndrome are;
 Characteristic malformations of the great toe & progressive heterotopic ossification.

    Atypical fibrodysplasia ossificans progressiva patients are categorized as fibrodysplasia ossificans progressiva–plus;
  Here the Patients either present with the classic features of FOP plus one or more atypical features (e.g. intercurrent aplastic anemia, craniopharyngioma, childhood glaucoma or growth retardation) (FOP plus), or present major variations in one or both of the two classic defining features of FOP (e.g., normal great toes or severe reduction deficits of digits) (FOP variants).

Diagnosis  The diagnosis of FOP is made by clinical evaluation. Confirmatory genetic testing is available.
      serum alkaline phosphatase activity and the erythrocyte sedimentation rate may be increased, especially during disease flare-ups.
      Urinary basic fibroblast growth factor levels may be elevated during disease flare-ups.
      Plain radiographs can substantiate more subtle great toe abnormalities and the presence of heterotopic ossification   

Outbreaks may be measurable clinically by elevated levels of alkaline phosphatase and bone-specific alkaline phosphatase

Differential Diagnosis; Osseous metaplasia,
                                      myositis ossificans,
                                      extraskeletal osteosarcoma.

Treatment
Unfortunately, there is no effective treatment for fibrodysplasia ossificans progressiva. Surgery is not an option for removing the excess bones because surgery often results in more bone formation. And these new bones don't disappear on their own.

• Preventative management is based on prophylactic measures against;

        - falls (e.g. improvement in household safety, use of protective headgear),
        - respiratory decline (e.g.incentive spirometry)
        - Viral infections
        - Avoid Deep Tissue Trauma: including intramuscular (IM) injections, if possible but venipuncture, subcutaneous & intravenous meds are OK
        - Take Intubation precautions: protect jaw and get expert anesthesia assistance since the jaw & neck may be completely or partially locked
        - Consulting of expert doctors is strongly recommended regarding potential risks of any surgical or medical interventions being considered.

• A brief 4-day course of high-dose corticosteroids, started within the first 24 hours of a flare-up, may help reduce the intense inflammation and tissue edema seen in the early stages of the disease.

• Medications also are available to help relieve symptoms of FOP, such as Narcotic analgesia & Muscle relaxants

The good news is that researchers are investigating FOP and new treatments. For example, a drug is being developed that may help to control bone growth.


Complications

•  Most patients with fibrodysplasia ossificans progressiva are confined to a wheelchair by the third decade of life and require lifelong assistance in performing activities of daily living.

•     Severe weight loss may result following ankylosis of the jaw.

•     Pneumonia and right-sided heart failure are complications of rigid fixation of the chest wall.

•     The severe disability of fibrodysplasia ossificans progressiva results in low reproductive fitness.

•     Death due to complications of thoracic insufficiency syndrome.

 Fibrodysplasia Ossificans Progressiva (Pictures Credit; reddit.)

 


NOTES;


1.  Connor JM, Evans DA (1982). "Genetic aspects of fibrodysplasia ossificans progressiva". J. Med. Genet. 19 (1): 35–39. doi:10.1136/jmg.19.1.35. PMC 1048816. PMID 7069743.

2.  Fibrodysplasia ossificans profressiva","Genetics Home Reference", February 18, 2014

3.  International Fibrodysplasia Ossificans Progressiva | www.ifopa.org

4.  Medscape| http://emedicine.medscape.com/article/1007104

5.  Philosophical Transactions of the Royal Society 41 (January, 1753): pp. 369 – 370.

6.  Pignolo RJ, Foley, KL. Non-hereditary heterotopic ossification. Implications for injury, arthropathy, and aging. Clin Rev Bone Miner Metabol. 2005;3:261-266.

7.  Segen's Medical Dictionary. © 2012 Farlex, Inc.

8.  Shore EM, Xu M, Feldman GJ, et al. A recurrent mutation in the BMP type I receptor ACVR1 causes inherited and sporadic fibrodysplasia ossificans progressiva. Nat Genet. May 2006;38(5):525-7.

9.  The Chirurgeons Apprentice | disturbing-disorders-fop-stone-man-syndrome

10. Wikipedia| Fibrodysplasia ossificans progressiva
  

Tree Man Syndrome , Lewandowsky-Lutz dysplasia or Epidermodysplasia verruciformis (EV)

Tree Man Syndrome

Lewandowsky-Lutz dysplasia or Epidermodysplasia verruciformis (EV)
This is an extremely rare autosomal recessive hereditary skin disorder associated with a high risk of skin cancer, characterised by marked susceptibility to Human Papilloma Virus HPV (type 5, 8) infection, which in the normal population is asymptomatic, but in these patients gives rise to scaly maculopapular lesions of the hands and feet, which have been fancifully likened to tree bark.

Tree Man Syndrome (Picture Credit; documentingreality)

It was First described by Felix Lewandowsky and Wilhelm Lutz in 1922, both dermatologists.

More than 200 cases have been reported in the literature so far.
Epidermodysplasia verruciformis is universal and affects persons of all races. No sexual preference is noted for epidermodysplasia verruciformis, although sex-linked and autosomal dominant inheritance have been described.

It has an onset of between the ages of 1–20, but can be seen in all age groups including children but the largest proportion is in patients aged 25-58 years (average 39 years).


 In people with a genetic predisposition, there is a mutation of chromosome 17 occurring within two genes – EVER2 or EVER1, which leads to lowering of the immunological potential of the skin, such that it becomes easily penetrable by HPV virus up to the deep layers of the skin and there is emergence of clinical symptoms, whereas this same Virus (in favorable genetic conditions) is tolerated by the immune system.

Risk factors include;

• immunosuppression, such as HIV infection, organ transplantation, or idiopathic lymphopenia,

• profound CD8+ T-cell lymphocytopenia

• Carcinogenic cofactors (e.g ultraviolet B and x-ray irradiation) are probably involved in the progression from benign warts (verrucae) to cancer.

Signs and Symptoms;

• progressive development of hyperpigmented or hypopigmented flat wart-like papules,

• irregular reddish brown plaques,

• seborrheic keratosis-like lesions and Tinea Versicolor like macules on the trunk and sun-exposed areas (neck, face, dorsum of hands and feet).

• Thick visible warts appear all over the body as well as on the inside of the skin.

• The skin becomes thick and hardened and as old skin dies new skin is created.

• The hands and feet, the extremities, are enlarged and it is difficult to use them.

• Hands and feet have been described as looking like contorted, yellow-brown branches extending up to 3 feet.

• Skin looks like tree bark or tree roots, hence the name Tree-Man Disease or Tree-Man Syndrome

Diagnosis of Tree man syndrome is suspected when this lesions are resistant to appropriate therapy. It is based on clinical and histological findings. Skin biopsy shows verruca plana-like lesions with mild hyperkeratosis, hypergranulosis and acanthosis of the epidermis. Keratinocytes of the upper epidermal layers are enlarged with perinuclear vacuolization and a typical blue-gray pallor.

Differential diagnosis include;
squamous Cell Carcinoma
Tinea Versicolor
Warts, Nongenital

Presently,there is no definitive treatment for Lewandowsky-Lutz dysplasia, however the following approach have been beneficial;

• Preventive measures like avoiding sunlight,UV-B exposure, UV-A exposure, and x-ray irradiation.

• Drugs like topical imiquimod and 5-fluorouracil, systemic retinoids, interferon, and 5-aminolevulinic acid photodynamic therapy. In advanced human papillomavirus (HPV)–related carcinomas, an experimental therapy involves treatment with a combination of 13-cis retinoic acid and interferon alpha or cholecalciferol analogues.

• Surgical and electrosurgical removal and cryotherapy are used in the treatment of benign and premalignant skin lesions. Surgery is also indicated for treatment of malignant lesions. If skin grafting is necessary, the graft should be from sun-protected skin.

Tree man syndrome (Picture Credit; pixshark)

NOTES;

1. Anadolu R, Oskay T, Erdem C, Boyvat A, Terzi E, Gurgey E. Treatment of epidermodysplasia verruciformis with a combination of acitretin and interferon alfa-2a. J Am Acad Dermatol. Aug 2001;45(2):296-9.

2. Bhawna Bhutoria, Kaushik Shome, Sulekha Ghosh, Koushik Bose, Chhanda Datta, and Subodh Bhattacharya. "LEWANDOWSKY AND LUTZ DYSPLASIA: REPORT OF TWO CASES IN A
FAMILY". Indian J Dermatol. 2011 Mar-Apr; 56(2): 190–193.

3. Gubinelli E, Posteraro P, Cocuroccia B, Girolomoni G. Epidermodysplasia verruciformis with multiple mucosal carcinomas treated with pegylated interferon alfa and acitretin. J Dermatolog Treat. Sep 2003;14(3):184-8.

4. Gül U, Kiliç A, Gönül M, Cakmak SK, Bayis SS (October 2007). "Clinical aspects of epidermodysplasia verruciformis and review of the literature". International Journal of Dermatology 46 (10): 1069–72.

5. Hoffner MV, Camacho FM. Surgical treatment of epidermodysplasia verruciformis. Dermatol Surg. Mar 2010;36(3):363-7

6. Majewski S, Jablonska S. Epidermodysplasia verruciformis as a model of human papillomavirus-induced genetic cancer of the skin. Arch Dermatol. Nov 1995;131 (11):1312-8.

7. Medscape | article; 1131981

PROGERIA , Hutchinson-Gilford Progeria Syndrome or "HGPS"

PROGERIA

 Hutchinson-Gilford Progeria Syndrome or "HGPS"

A rare congenital childhood disorder marked by gross retardation of growth after the first year and by rapid onset of the physical changes typical of old age, usually resulting in death before age 20. Also called premature-senility syndrome


           

First Black Child With Progeria. (picture credit; cbsnews)

 The word progeria comes from the Greek words "pro", meaning "before" or "premature", and "gēras", meaning "old age"    Progeria = "prematurely old."

It was named after the doctors who first described it; Dr. Jonathan Hutchinson, 1886 and Dr. Hastings Gilford, 1897.

While there are different forms of Progeria, the classic type is Hutchinson-Gilford Progeria Syndrome.

 Approximately 140 cases have been reported in medical history. However, the Progeria Research Foundation believes there may be as many as 150 undiagnosed cases worldwide.

There is a reported incidence of Progeria of approximately 1 in every 4 to 8 million newborns. Both boys and girls run an equal risk of having Progeria. Progeria appears to affect children of all races equally.

Here there is a de novo mutation leading to autosomal dominant single base substitution in the Lamin A gene. The expression of this mutated Lamin A gene results in a truncated protein known as 'Progerin'. In HGPS there is an excessive accumulation of Progerin that is toxic to cells, causing DNA damage and genomic instability.

 When cells use this protein, called progerin, they break down more easily. Progerin builds up in many cells of kids with progeria, causing them to grow old quickly.

Progeria is not inherited, or passed down in families as children who suffer from it rarely live up to their reproductive age.
Children with progeria generally appear normal at birth.
Although they may come from varying ethnic backgrounds, children with Progeria have a surprisingly similar appearance.

signs and symptoms include;

•      A bigger head

•      Large eyes incomplete closure of the eyelids

•     A small lower jaw, thin lips and beaked nose

•     Ears that stick out

•     Slow and abnormal tooth growth, with below-average height and weight

•     Loss of body fat and muscle

•     Hair loss, including eyelashes and eyebrows

•     Narrowed face,

•     Head disproportionately large for face

•     Thinning, spotty, wrinkled skin

•     Visible veins

•     High-pitched voice

•     Hardening and tightening of skin on trunk and extremities (similar to scleroderma)

•     Some hearing loss

•     Fragile bones

•     Stiff joints

•     Hip dislocation

•     Insulin resistance

•     Severe progressive heart and blood vessel (cardiovascular) disease

Physical appearance is highly suggestive of the diagnosis and it can be confirmed through a genetic test for LMNA mutations.


Presently,there is no known cure for Progeria, though a cancer drug "farnesyltransferase inhibitors"(FTIs), is still under clinical trial and results showed significant improvements in bone structure, weight gain, and the cardiovascular system.

Treatments usually help ease or delay some of the disease's symptoms.

Drugs to lower cholesterol or prevent blood clots can be prescribed. A low dose of aspirin every day can help prevent heart attacks and stroke. Growth hormone can help build height and weight.

Physical and occupational therapy can help keep the child moving if they have stiff joints or hip problems.

First Black Child With Progeria. (picture credit; cbsnews)

Surgery; Some children may have coronary bypass surgery or angioplasty to slow the progression of heart disease.

Kids with progeria are more likely to get dehydrated, so they need to drink plenty of water, especially when they're sick or it's hot. Small meals more often can help them eat enough, too. Cushioned shoes or inserts can ease discomfort and encourage the child to play and stay active.

Those born with progeria have a live span of between 8-21 years, the average being 13 years.

There are other progeroid syndromes that run in families. These inherited syndromes cause rapid aging and shortened life span:
 1. Wiedemann-Rautenstrauch syndrome, also known as neonatal progeroid syndrome, starts in the womb, with signs and symptoms of aging apparent at birth.
 2. Werner syndrome begins in the teen years or early adulthood, causing premature aging and conditions typical of old age, such as cataracts and diabetes.



NOTES:

1.  The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company.

2.  Ewell Steve Roach & Van S. Miller (2004). Neurocutaneous Disorders. Cambridge University Press. p. 150. ISBN 978-0521781534.

3.  Hennekam RC (2006). "Hutchinson-Gilford progeria syndrome: review of the phenotype". Am. J. Med. Genet. A 140 (23): 2603–24.

4.  Hutchinson J (1886). "Case of congenital absence of hair, with atrophic condition of the skin and its appendages, in a boy whose mother had been almost wholly bald from alopecia areata from the age of six". Lancet I: 923

5.  Kwang-Jen Hsiao (1998). Advances in Clinical Chemistry:33. Academic Press. p. 10. ISBN 0-12-010333-8.

6.  MayoClinic | progeria

7.  Progeria Research Foundation 

8.  WebMD | progeria

9.  Wikipedia |  Progeria

STONE BABIES (Lithopedia)

STONE BABIES (Lithopedia)


This is a rare medical phenomenon, as at date, Only about 300 cases have been reported or documented. It Was First described by Dr Albucasis (an Arab Muslim physician and surgeon who was the first physician to describe an ectopic pregnancy, and the first physician to identify the hereditary nature of haemophilia).

Lithopedion; a fetus that has died during an ectopic pregnancy (pregnancy outside the Uterus,in this case mostly abdominal pregnancy) and has become calcified, ossified or hardened. It may remain undiagnosed for decades. Also called calcified fetus, lithopedium, ostembryon, osteopedion. Lithopedia; plural.

Lithopedion ( Picture Credit: citizenpost. )

Tends to occur in abdominal pregnancies as opposed to intrauterine pregnancies, even though it is possible for the fetus to remain within the uterus.. A tubal pregnancy can result where the fetus grows within the fallopian tube and rarely the fertilized egg will escape the end of the fallopian tube and settle within the abdomen.
Sometimes the blood supply is established and the child can grow within the abdomen, rarely to term but it can grow. It would take 12 weeks or more for the fetus to reach a size that would be easily visible.

About 1.5 and 1.8% of abdominal pregnancies develop into lithopedia.

Here,the tissues of the dead fetus are too large to be absorbed by the body, so they are walled off as foreign bodies with fibrous tissue and this most often Calcify which is where the term stone baby comes from.

The development of lithopedion happens under certain conditions:
(1) extra-uterine pregnancy;
(2) fetal death after 3 months of pregnancy;
(3) the egg must be sterile;
(4) there cannot be any early diagnosis;
(5) local conditions must exist for calcium precipitation (deposit)

Most times it occurs without symptoms (Asymptomatic) and is discovered incidentally following an Abdominal X-ray taken for some other reason, as the only symptom may be the feeling of discomfort, sensation of a mass or fullness in her abdomen.

Here the woman could have normal Menstruation, and could even become pregnant again since the uterus, ovaries, and fallopian tubes would be normal and would continue to function normally.

However, if the fetus remained within the uterus, this could interfere with future pregnancies, though not always.
It would be very similar to a woman who had large fibroids, which are muscular masses that develop with in the muscular wall of the uterus and often cause pain and abnormal bleeding. Sometimes normal pregnancies occur despite these.

Some associated complications have been reported after a long asymptomatic evolution: urinary bladder and rectum perforation; extrusion of fetal parts through the abdomen wall, rectum and vagina; intestinal obstruction (due to collision of fetal parts with the intestine or adherence), abscess formation and volvulus.

Treatment is by surgical extirpation/removal.


NOTES;

1. Costa SD, Presley J, Bastert G. Advanced abdominal pregnancy. Obstet Gynecol Surv 1991;46:515-25.

2.  Frayer CA, Hibbert ML. Abdominal pregnancy in a 67-year-old woman undetected for 37 years: a case report. J Reprod Med 1999;44:633-5. 

3.  Irick MB, Kitsos CN, O'Leary JA. Therapeutic aspects in the management of a lithopedion. Am Surg 1970;36:232-4.

4.  Mishra JM, Behera TK, Panda BK, Sarangi K; Behera; Panda; Sarangi (September 2007). "Twin lithopaedions: a rare entity". Singapore Medical Journal 48 (9): 866–8. PMID 17728971.

5.  Mosby's Medical Dictionary, 8th edition. © 2009, Elsevier.

6.  Passini, Renato; Knobel, Roxana; Parpinelli, Mary Ângela; Pereira, Belmiro Gonçalves; Amaral, Eliana; de Castro Surita, Fernanda Garanhani; de Araújo Lett, Caio Rogério (November 2000). "Calcified abdominal pregnancy with eighteen years of evolution: case report". São Paulo Medical Journal 118 (6): 192–4.

7.  Spiritos NM, Eisenkop SM, Mishell DR. Lithokelyphos: a case report and literature review. J Reprod Med 1987;32:43-6.