Gallstone (Obstructive jaundice)

Patient is a 31 years old Malay lady, P1, LNMP 2/52 with no known underlying medical illness presented with abdominal pain over 1 week prior to admission with history of similar pain 3 weeks ago.

For the first episode which has occurred last 3 weeks, the pain was in epigastric region, radiated to right and left hypochondriac.  There was no other associated symptoms. She the presented to a hospital in her district for treatment. She was diagnosed with gastritis and was prescribed with gastritis medication. She claimed the pain was relieved.


One week prior to admission, she had recurrent episode of pain similar in character as last 3 weeks. She described the pain as throbbing in nature, persistent and increased in intensity. Pain was aggravated by movement with no specific relieving factor with pain score of 6-7/10. However it was associated with tea vomiting, about 2 to 3 times a day. Vomitus contained food particles with fluid, with no bile or blood.

On further questioning, she also started to notice yellow discoloration of her sclera and skin for 3 days prior to admission. She also complained of having tea-colored urine and pale colored stool for one weeks and itchiness on her arm and abdomen.

Cholestasis means "the slowing or stopping of bile flow" which can be caused by any number of diseases of the liver (which produces the bile), the gallbladder (which stores the bile), or biliary tract (also known as the biliary tree, the conduit that allows the bile to leave the liver and gallbladder and enter the small intestine). When this occurs, conjugated bilirubin and the waste products that usually would be cleared in bile reflux back into the bloodstream. This causes a primarily conjugated hyperbilirubinemia and jaundice; the liver conjugates the bile to make it water-soluble and because the bile has already been processed by the liver, when it gets backed up because of a blockage and is refluxed into the blood, the blood will have high levels of conjugated bilirubin. This is in contrast to primarily unconjugated hyperbilirubinemia which is the water-insoluble form that is bound to serum albumin; the liver has not had a chance to conjugate the bilirubin yet and can be caused either because too much unconjugated bilirubin is made (such as in massive hemolysis or ineffective erythropoiesis) or because too little is conjugated (Gilbert's disease or Crigler-Najjar syndrome). Unconjugated hyperbilirubinemia does not typically cause pruritus.
It is thought that bile acids that deposit into the skin is responsible for the pruritus (itching) but the levels of bilirubin in the bloodstream and the severity of the pruritus does not appear to be highly correlated

Claimed to have history of flatulence dyspepsia but was unsure since when. There was no history of fever with chills and rigor, no chest pain, shortness of breath, palpitation and no acid reflux symptoms. 

Patient presented to nearby hospital in her district, there she was infused with intravenous fluids, analgesics and her blood was taken taken for investigations. She then was referred to here for further investigation and management.

There was no other significant surgical history except for emergency lower caeserian section 6 months ago due to failure of induction of labour. Surgery went well, and she denied postoperative complication. She denied taking oral contraceptive pills.

Her mother was diagnosed with diabetes mellitus on insulin and hypertension which is well-controlled. Her father died 10 yers ago due to infection. There was no history of malinancy or similar problem in family.


She is a factory worker married to a FELDA settler. Their total income is around per month, claimed to be adequate for basic necessaries. Her husband is a smoker. Both partners denied alcohol consumption.

Upon clerking, she was alert and concious. She looked lethargy and in pain. She was jaundiced with poor hydrational status. A branulla was attached on her forearm, and she was infused with flagyl solution. She was on urine bladder catheterization, containing 400 ml dark tea-colored urine. Otherwise , no pallor, spider naevi, koilonichia, clubbing, palmar erythema and ankle edema.

She was on CBD. If someone is presented with sign and symptoms suggestive of obstructive jaundice, they will be put on CBD, not to merely look at the changes, but the most crucial part is to monitor if patient developed sepsis. In cases of obstructed biliary tree like choledocholethiasis, we afraid if patient complicated with ascending cholangitis (possible to develop). Ascending cholangitis is a medical emergency which can develop into sepsis.

Abdomen was not distended and inverted, there is scratch mark seen at the epigastric region. There was a well-healed suprapubic scar measured about 18 cm. No dilated veins seen and hernial orifices were intact. On light palpation, the abdomen was soft and revealed tenderness on the apigastric, right and left hypochondriac regions. Murphy's sign was negative. (In chronic cholecystitis for example, there might be tenderness at RUQ but merely tenderness with no cacthing of breath and painful expression by patient are not Murphy's sign. Murphy's sign should be specfic and sensitive for acute cholecystitis. Liver span was 12 cm. There was no hepatosplenomegaly and no palpable mass. Auscultation and percussion showed no significant finding.

Per rectal examination reveled empty rectum with normal smooth mucosa.

There is almost always tenderness and guarding in the right hypochondrium. Palpate the abdomen just below the tip of the ninth costal cartilage and ask the patient to take a deep breath.When the liver and the attached gallbladder descend and strike the palpating hand, the patient will experience a sharp pain which prevents further inspiration.This is called Murphy’s sign. " -Browse’s Introduction to the Symptoms and Signs of Surgical Disease-

Provisional diagnosis
Choledocholithiasis

Ddxes
-acute pancreatitis
-biliary tumor
-ascending cholangitis

Investigation and management 

Laboratory investigation was ordered for 

• Arterial blood gases
• monitor any respiratory distress
• Full blood count
• white blood cell count
• Renal profile 
• Liver function test
• coagulation profile
• to assess any coagulation defect  
•  If biliary tract is obstructed
• Bile, which is an emulsifying agent, tolong pancreatic lipase to hydrolyse the lipids from foods, cannot reach duodenum
• Lipids not digested..not absorbed
• Leading to passage of loose, pale, foul-smelling fatty stools (steatorrhea) 
• Logically, the fat soluble vitamins also are not absorbed (ADEK)
• Lack of vitamin K leads to inadequate prothrombin synthesis
• Hence defective clotting
• Random blood sugar 
• UFEME

She was then infused with intravenous isotonic solution. *read more on the regimes later*.
She was given 

• cefobid *read more on cephalosporin drugs*
• 
  
• flagyl
• tramadol and paracetamol (PCM)
• analgesic
• please refer local procedure

• PS 0-3	4-6	7-10
  mild	moderate	Severe
  PCM	PCM and tramadol	Morphine +/- (PCM/tramadol)

• omeprazole : peptic ulcer inhibitor
• antidiabetic (WHYYY??? ASK DOCTOR LATER, FOLLOW UP THIS PATIENT)
• metformin
• glibenclamide

Ultrasound of heptobiliary system and abdomen was done revealed impression of chronic cholecystitis and gallstone. But remember the patient already presents with sign and symptoms of obstructive jaundice.

• stone in gall bladder with sludge seen
• gall bladder contracted with thickened gall bladder wall

Completed IMRIE score was done revealing mild pancreatitis.

The patient was planned to undergo ERCP on the third day of admission.

Spectrum of diseases in gall stone

Spectrum of diseases in JAUNDICE

1) malignancy- any malignancy along the hepatobiliary tract, metastases tumor, tumor that metastases to lymph node at porta hepatis, lymphoma etc
2) infections-divide into bacterial, viral, parasite (worm can migrate and block the pathwa)
3) trauma
4) congenital - congenital haemolytic anaemia such as thallasemia, g6pd def, hereditory spirocytosis, wilson disease etc
5) drug induce
6) stone (not fit in any cause)

Spectrum of diseases specific in Obstructive jaundice

1)congenital : choldedocal cyst, biliary atresia

2)infection : ascending cholangitis

3)malignancy

4)iatrogenic

5)miscellaneous : stone

WHAT IS COURVOISIER’S LAW 

There a lots of pictures available in the google or books which illustrate nicely, summarizing the formulation behind this law. My reference was from Burkitt Essential Surgery, my favourite surgery bible so far. Recommended.

References 

Burkitt, H.G, et. al, Essential Surgey: Problems, Diagnosis & Management(2007), Fourth Edition., 

N.L, et. al, Browse’s Introduction to the Symptoms and Signs of Surgical Disease(2005), Fourth Edition, Hodder Arnold, UK.

Urinary obstruction in pregnancy

Patient, a 39 years old Malay , G4P3 currently at 16 weeks period of amenorrhea  presented with difficulty in urination over 2 weeks. She has no known underlying disease. This was a referred case from Hospital X.

She described that she started to have difficulty in urination in which she need to strain to urinate since last two weeks. It was associated with pain during urination. She described that stream was slow and after micturition, she felt her bladder was not voided well. There was also post-micturition dribbling and she need to wake up at night to go to the toilet. She then decided to use diaper to avoid her from going to toilet too often.

A week ago, she started to experience mild suprapubic pain and tenderness. She noticed that her abdomen is distended as if as her pregnancy was more than 16 weeks. The pain was localized to the suprapubic area, and the suprapubic area became hard and warm with no redness.

Patient then went to nearby hospital in her district, Hospital X at emergency department. She was not admitted but was prescribed with potassium citrate and no other procedure was done. However she symptoms did not subside and the pain worsened, described as 5-6/10. She then started to notice that her urine became cloudy with fishy smell. She denied any other abnormal discharge. It was not associated with fever and there was no changes of bowel habit. She denied any lost of weight or lost of appetite. The was no similar episode of complaint before.

After about a week, she went for her regular antenatal visit in Klinik Kesihatan Y. There, she was told that her SFH was like 26 weeks. Urine test was done showed proteins and white blood cells and her Hb was 8.6 which is low. On the same day, she was referred to Hospital X and immediately was put on CBD to void her bladder, relieving the suprapubic pain and the area became softer. There was blood in her urine but on further questioning, she claimed not to have any anemic symptoms such as palpitation, dizziness, shortness of breath or chest pain.

Ultrasound was done afterwards showed all parameters corresponded to 16 weeks with no abnormality. Fetal movement was good. In Hospital X, she was given intravenous cefuroxime and Ural powders before being sent to Hospital AAA for further investigation and management.

This is how ural sachet looks like. Usually the patient will say " ubat minum tu serbuk macam ubat ENO tu, doktor."

It is a urine alkalinizer, which means it will add base to urine to neutralize it. When acid is neutralized there are fewer H+ molecules, hence the pH rise. Human urine can have pH ranging from about 4 (acid) to about 8 (alkaline). When pH increase, stone will become mores soluble.

PotCit. Most patients are not compliant to this anyway. It tastes suck. 

But, potassium if kidney function is deranged, watch out before prescribing PotCit.

On general examination, patient was alert, concious and pink She was not tachypneic and not in pain. Hydrational and nutritional status was good. Vital signs are normal. There was one branula attached on dorsum of left hand but she was not on any intravenous infusion. She was on catheter which was connected to a reservoir bag containing 1L Sodium chloride 0.9% solution and a CBD bag which contained 600ml haematuria with no clots. Abdomen was slightly distended with cutaneous signs of pregnancy ; linea nigra. On palpation, the abdomen was generally soft but tender at suprapubic area. SFH was 15cm, corresponded to period of amenorrhea. No mass palpable per abdomen. Per rectal examination was not done.Examination of other systems reveal no abnormality.

Management

Few investigations was done

1. Full blood count
• to look for Hb level as she has hematuria after the CBD was inserted
• platelet because of the hemuria
• any leucocytosis which may signify an ongoing infection or inflammation
2. Coagulation profile
3. UFEME
• any trace of protein, leucocyte, nitrite, erythrocyte
• culture and sensitivity
4. Renal profile + albumin

Upon clerking, CBD was already changed once. During the changing, the catheter was changed form 2 ways to 3 ways catheter as the haematuria is not resolving. 3 ways catheter is for bladder irrigation. She can take orally, hence there was no need for isotonic solution infusion. Cefuroxime was given intravenously (antibiotic) with Ural, a urine alkalinizer. 

3 ways

2 ways

Bladder irrigation
Source : http://what-when-how.com/wp-content/uploads/2012/08/tmp325129_thumb22_thumb.png

She was planned for

1. ultrasound KUB to look for any stones, or dilatation.
2. Cystoscopic examination 

In her case of urinary obstruction and frank hematuria, the urologist planned to rule out bladder cancer. It can also be due to traumatic hematuria secondary to catheter insertion." Apart from the direct trauma due to the technique, the catheter itself can sometime cause irritation to bladder mucosa in certain patient. It is usually mild and not require any intervention. All you need to do is to observe the condition and KIV for bladder irrigation if not resolving." -DrJackNaim'sNotes-

Urinary catheter is used to drain bladder

Indications are :

• Urinary incontinence 
• Urinary retention 
• Surgery on the prostate or genitals
• Prolonged immobilization
• Other medical conditions such as multiple sclerosis, spinal cord injury, or dementia

Provisional diagnosis : Bladder in stone (cystolith)

DDxes :

• bladder cancer
• urethral stricture
• pelvic mass

Shock

As usual, after I clocked in at the department, I go to level 1 and saw my colleagues lepak2 bersenang lenang at the tables provided in the hallway, ate nasi lemak ayam or nasi minyak in the morning dua ringgit setengah. The group which will be presenting was setting up their seminar on the day, Shock, supervised my Mr. Khadri. It sounds like a simple seminar indeed, revising things which was taught in each year since our first year in medical school. But still, there were lots of knowledge we are lacking.

In any medical or surgical textbooks, shock is among the earliest topic the author or editor would put into their books. It should be in the second or third chapter, like that. In any posting, be it in O&G, medical, ortho, paed, surgical, shock is a very important topic which is mandatory to be covered. It can happen everywhere and anywhere even if one day one of you happen to be a clinical pathologist, looking at specimens day and night sampai juling, if your title is doctor, shock is still a thing you should not throw it away from your cerebrum, lock it deep inside. Unless, you want to start to do other business, then you may go and throw it away.


Basically, the presenters were presenting the same thing back in our BMS, refreshing our mind on what we have learnt. The definition, in a simple way in my language

"Profound haemodynamic and metabolic disturbance characterized by failure of the circulatory system to maintain an appropriate blood supply to the microcirculation with the consequence of inadequate perfusion of vital organs."

In a simple way, systemic hypoperfusion of tissue of organs, so they shut down la...dah tak ada modal, nak jalan pun tak boleh. Like a factory.

So, they classified shock pertaining to its etiology which lead to inadequate perfusion

• cardiogenic
• hypovolemic
• distributive
• anaphylactic
• neurogenic
• septic

The pathophysiology from inadequte perfusion in each etiology which will eventually lead to organs failure.

http://upload.wikimedia.org/wikipedia/commons/thumb/0/0e/Shock-cell2.svg/500px-Shock-cell2.svg.png

The stages of shock together with the clinical features in each stage. They are almost the same, but might be different in the distributive type wherein there will be pooling of blood to the periphery.

Complication of shock was included as well, spesific for each organ. Commonly, in the ward, kidney is the first to be affected.

And a lot more. I was yawning throughout the seminar, I couldn't sleep last night as usual. My eyes was like satu suku lagi boleh tutup dah, but I tried to keep it open and yes, my eyes wide opened when the last presenter mentioned " Any question?" Heh.

So, they were bombarded with questions. Honestly I was waiting for the presenters to discuss on the management and complication in clinical point of view, yes they did but not as complete as I thought. I was expecting more, ended up, I put it as my learning need and will do more reading on that later. Biyane... :P But, it was a great seminar though, Come on, we are still new whaaaatt. *Excuses* 

Few questions was asked and more questions came as the discussion went on.

1. What if localized inflammation with no systemic manifestation but presented with shock? 
2. At what stage resuscitation should be done? 
3. What is PCWP (pulmonary wedge pressure)? how is the procedure done? Is it commonly used in our local setting? 
4. management of shock especially in case of hypovolumic shock and the importance of clinical judgement in managing and recogniczing shock. Is blood transfusion is more superior than isotonic solution?

Discussion 

1. We know that shock is set in motion when there is failure to deliver towards and to excrete substances away in short. But how does that occur in a person would be depending on two factors 

• insults which was presented well by the presenters pertaining to the etiology.
• body response is different between persons. A patient may come with small amount of insult like a simple cat-scratch but may develop severe shock. A patient may presented with many cat-scratch or bites ( huh?) but still nothing happen.

For example, in case of bleeding or trauma

Case 1 : A 65 year old gentleman with several co-morbidities namely ischemic heart disease, kidney disease, etc. lost blood about 500 ml but may presented with late stage of shock.

Case 2 : A young, medium built gentleman with no known medical illness, lost 1 500 ml ( sebotol air mineral besar) may come with just dizziness, or showing early stage of shock.

http://www.dcavm.org/10oct2.gif

Even if we were provided with several guidelines of the clinical features of shock, the doctors will decide if this is shock or not. Early recognition is very crucial and should not be missed as it may affect if the treatment will be successful.

Cardinal signs of acutely ill or shocked patient

• substantially increased or decreased respiratory rate
• bradycardia or tachycardia
• low BP
• hypo or hyperthermia
• decreased level of consciousness

REFER MEWS

2. At what stage resuscitation should be done? Once shock is recognized, resuscitation need to be done, stabilizing every components ABCDE.

Early management should be within 24 hours  of acute deterioration

• clinical assessment of the volume
• treat the cause of shock or infection if any
• support vital organs
• optimise the cardiovascular and haemodynamic system, aiming for 
• central venous pressure 8-12mmHg
• mean arterial pressure over 65mmHg
• UO >0.5ml/kg/hour
• monitor and assess the response
• urine output
• stroke volume

3.Blood is not the best for resuscitation. The best is by using isotonic such as D5%, NS, HM, etc \ but need to remember, HM solution contain lactate which might worsen acidosis in shock.

May Allah ease.

Fat Embolism

Just now, I shared something I gained from a ward round, there was an ortho team came and taught me something which is

2 most common causes of chest pain among hospitalised  patient
1. Pneumonia
2. Pulmonary embolism.

In case of mva cases for example  if the chest pain develop veeeeryyy suddent, may suspect fat embolism  in case of fractured bone. So the discussion went on with my colleagues and senior on fat embolism when she said that in ortho, lecturers love to ask 

• how to diagnose fat embolism? 
• What are the criteria? 
• What is the definitive way to diagnose fat embolism?

Kak Maliya asked us but answered them herself. LOL. because we are not posted to ortho yet. Butt, this is important isn't it to know the pathology as a whole. Here are the discussion

FAT EMBOLISM SYNDROME

Fat embolism is a common phenomenon following limb fractures. Circulating fat globules larger than 10 μm in diameter occur in most adults after closed fractures of long bones and histological traces of fat can be found in the lungs and other internal organs. A small percentage of these patients develop clinical features similar to those of ARDS; this was recognized as the fat embolism syndrome long before ARDS entered the medical literature. Whether the fat embolism syndrome is an expression of the same condition or whether it is an entirely separate entity is still uncertain. The source of the fat emboli is probably the bone marrow, and the condition is more common in patients with multiple fractures.

Clinical features

Early warning signs of fat embolism (usually within 72 hours of injury) are a slight rise of temperature and pulse rate. In more pronounced cases there is breathlessness and mild mental confusion or restlessness. Pathognomonic signs are petechiae on the trunk, axillae and in the conjunctival folds and retinae. In more severe cases there may be respiratory distress and coma, due both to brain emboli and hypoxia from involvement of the lungs. The features at this stage are essentially those of ARDS. There is no infallible test for fat embolism; however, urinalysis may show fat globules in the urine and the blood PO2 should always be monitored; values below 8 kPa (60 mmHg or less) within the first 72 hours of any major injury must be regarded as suspicious. A chest x-ray may show classical changes in the lungs.

Management

Management of severe fat embolism is supportive. Symptoms of the syndrome can be reduced with the use of supplemental high inspired oxygen concentrations immediately after injury and the incidence appears to be reduced by the prompt stabilization of long-bone fractures. Intramedullary nailing is not thought to increase the risk of developing the syndrome. Fixation of fractures also allows the patient to be nursed in the sitting position, which optimizes the ventilation–perfusion match in the lungs.

Reference: Apley (aka Ortho Bible in UIA)


From the "clinical features" in the text above, what are the things you monitor in ward? Keep an eye on the body temperature and pulse rate, and also respiratory rate. Also, GCS, SpO2. KIV arterial blood gas, urinalysis, and CXR (nak ambik tapi tak tau wajib ke tak, takut bazir duit kerajaan). Document whether any petechiae seen on trunk, axillae, and conjunctival folds.

Mortality rate of fat embolism : 5-15% which is high 

Petechiae tu dah late/severe stage.

Management is supportive, mcm patient acute pancreatitis, banyak fluid, avoid dehydration. And oxygen

Diagnosis is clinical. Kalau nak definitive diagnosis, kena buat autopsy. Seperti amniotic fluid embolism masa O&G tu.

pathogenesis of petechia in fat embolism?

"The characteristic petechial rash may be the last component of the triad to develop. It occurs in up to 60% of cases and is due to embolization of small dermal capillaries leading to extravasation of erythrocytes. This produces a petechial rash in the conjunctiva, oral mucous membrane, and skin folds of the upper body, especially the neck and axilla. It does not appear to be associated with any abnormalities in platelet function. The rash appears within the first 36 h and is self-limiting, disappearing completely within 7 days."

Source: http://m.ceaccp.oxfordjournals.org/content/7/5/148.full

Is is Gurd's criteria

photo courtesy : kak Maliya

Sign and Symptoms of metastases (the common sites)

Manifestation would be depending on the site of metastases. It is true that cancerous cell can metastases like almost everywhere it wants, hijacking anywhere they are settled in. But there are favored organs or site which are commonly found, probably due to receptor-molecular-blah-blah thingy. If you know it, it is a bonus then.  Sometimes, the sign and symptoms of metastases might be found much earlier. 

1. Lymph node

• Lymphadenopathy which is not mobile as it commonly is fixated, irregular margins and any characteristics which are suggestive of malignant lumps. But, if the location is intraabdominal, I t can only be visualized by imaging unless if it get soooooo big.

• Sentinel lymph node is the first site of LN which are first to be infiltrated. How do they know it is the sentinel LN is by injecting radioactive liquid into tumor  which nodes got colored via scan.

• Nontender

2. Liver

• Jaundice as it deposited in liver

• Hepatomegaly- abdominal discomfort

• Obstructive jaundice can also be caused by extensive liver deposits or LN in porta hepatis compressing the bile duct

3. Lung

• Cough 

• Hemoptysis

• SOB due to pleural effusion --->Collection of fluid in the pleural space

o Trachea and apex beat displaced away from a massive effusion

o Expansion reduced on affected site

o Stony dullness over the fluid

o Breath sounds reduced or absent

o Vocal resonance reduced

4. Bone

• Pathological fracture

• Bone pain

• Sometimes may cause stenosis of it affect vertebrae and compressing the spinal cord. Patients may come with weakness of lower limbs bilaterally if it compressing the lumbar parts. Look for any bowel incontinence or urination habit is altered as that may signify compression of cauda equina. Do more reading on that!

5. Brain 

• Headache

• Blurred vision

• Seizure

• Limb weakness

• Paresis, ataxia

• Behavioral or personality changes

• SSx of space occupying lesion 

6. Other common sites are peritoneum or adrenal glands.

References :

1. Talley O connor Physical Examination textbook
2. Burkitt, H.G, et. al, Essential Surgey: Problems, Diagnosis & Management(2007), Fourth Edition.

Projectile vomiting in GERD???

We were discussing with an MO on atypical SSx of GERD whether projectile vomiting can occur in GERD.

Referring to Prof nasser notes during bms, increased intracranial pressure can cause projectile vomiting but the pathophysiology behind that is unclear.

GERD is mainly due to problem with antireflux barrier, primaryly lower esophagal sphincter. So increase  in intrabdominal pressure can cause vomiting in GERD. But the classical symptoms of GERD is heartburn and epigastric pain.

Atypical   symptoms  are vomiting, dental enamel erosion, respiratory ssx, ear nose throat symptoms, n chest pain...chest pain unusual and nonspesific.

However, GERD can be associated be preceded / contributed by increased abdominal pressure which might lead to vomiting but symptoms are heartburn and dyspepsia. It is called as reflux esophagitis, not up to projectile vomiting.

GERD that presented with projectile vomiting are in small children & infant as the causes mainly underlying weak LES...the stomach is small and esophagus tract is shorter compared to adult...with the amount of food / fluid that the infant take. So it may reflux and shoot up as projectile. Nevertheless projectile vomit in children or infant with GERD is not that common & pyloric stenosis or obstruction have to be ruled out.

http://www.hon.ch/OESO/books/Vol_5_Eso_Junction/Articles/Images/140f1.jpg

http://www.hon.ch/OESO/books/Vol_5_Eso_Junction/Articles/Images/140f1.jpg

Oesophagal cancer presented with Dysphagia

To be honest I really like surgical posting so far. Because when I was in BMS, (basic medical sciences) ,we were not really exposed to O&G cases in our problem-based learning (PBL). So when i was first posted in O&G department in my clinical years, I was like WHAAAATTTHAAAA...But it was fun, ikhlas. Hik2.

Different with the current posting, we were given few cases which can be found in surgical ward, colorectal cancer, oesophagal cancer, intestinal obstruction,[list goes on and on]. So it is really exciting to be able to clerk a real patient with real findings which was taught before in theory classes, which you usually can only see in books. But, it is not like that all the time, clinical judgement might varies... and very individual basis. Not all said symptoms will be there for a particular disease, hence diagnosis making really make my anxiety go through the rooftop during case presentation with fierce specialist.

Here is a case of oesophagal cancer! :)

*express consent was gained for educational purpose, might be altered and not completed to avoid breaching the confidentiality* 

History ( Somewhat the summary)

Madam X, a 50 y/o lady with no known underlying disease admitted to the ward due to difficulty in swallowing over 3 months.


She was apparently well until last 3 months when she started to experience difficulty in swallowing rice or chicken. Later, she began to have difficulty in swallowing semisolid food namely porridge. Very recently he began to have choking sensation upon swallowing. It was associated with vomiting shortly after eating. The vomiting was not projectile and not associated with nausea, abdominal pain, and headache. Vomitus was undigested foods with fluid with no blood or bile.

She began to have pain upon swallowing last 2 months which occur the food reach at the level of 3rd rib.The pain doesn't radiate elsewhere and limited during swallowing only, making it difficult tolerate oral intake or swallowing saliva. Pain score was 5-6/10.
Recently, she complained of passing out coal-black and sticky stool.

She denied having lower retrosternal pain, regurgutation, haematemesis, abdominal swelling, jaundice or fever, hoarseness of voice, hiccups.
She claimed to have lost of appetite and lost of weight about  20kg over a period of 3 months. There was no sign and symptoms of metastases. ( I will explore on this later in another post).
She was once went to a clinic due to the persisting condition last 3 weeksand was given medication but was unsure what was the prescription but she claimed the symptoms did not resolved.


She was a chronic tobacco smoker since teenager and stopped 3 months ago. She claimed that she did consume betelnut (sireh, a risk for nasopharyngeal ca as well), but denied consuming alcohol.

Discussion on dysphagia

Dysphagia should not be confussed with globus pharyngeus( lump in throat sensation)


The characteristic sof dysphagia should be detailed on further questioning, which is not only important to look for causative pathology but also crucial for the decision of managemenht whether the patient might need immedieate admission, treated as outpatient, TCA or considered as medical emergency especially inability to swallow saliva ( mati tercekik air liur, kau nak jadi gitu??)

 Causes, (find out yourself)

1. oesophagal motility such as achalasia (is a failure of smooth muscle fibers to relax, which can cause a sphincter to remain closed and fail to open when needed). Last time I tagged a surgery consultant in a hospital at surgical out patient. There was 16 y/o girl was diagnosed with achalasia, bringing along oesophagometry result with her. The consultant suggested her several treatment which includes fundoplication, cardiomyomectomy, because long term effect would be fatal.

2. extrinsic pressure may include mediastanal gland, goitre, enlarged left atrium


3. intrinsic lesion like malignancy, stricture

4. disease on mouth and tongue, difficult to initiate swallowing, lead to drooling

5. foreign body

Clinical Manifestation of Oesophagal cancer

1. early stage

• dysphagia ( most common), should be progressive
• weight loss in more than 50% of people with esophagal ca.

2. cancer progress

• bleeding, haematemesis, or malena
• hoarseness of voice caused by invasion of recurrent laryngeal nerve or compression onto it, making resection less possible
• pain may be felt in epigastric or retrosternal area. Pain on bony structures indicates metastatic disease
• persistent cough
• respratory sysytem : like shortness of breath (SOB) can be due to aspiration of undigested food or by direct invasion of tracheobronchial tree by tumour

3. Late stage

• may completely block the esophagus
• swallowing becomes impossible, regurgitaion and drooling as secretion build up in the mouth

Two types with different risk factors

1. squamous cell carcinoma

2. adenocarcinoma ( may occur in longstanding GERD and Barret esophagus)

References : 

1. crash course surgery

2.Merck Manual

3. medscape

Refer burkitt and talley for proper reading.

Leiyomyoma

Leiomyoma, as it is named is a benign tumor arising from uterine smooth muscle.  It is also can be termed as may contain fibrous tissue giving it a firm consistency. It is a common tumor that can cause heavy menstrual bleeding, pelvic pressure symptoms and reproductive disorders.

Histological findings usually show a whorled of smooth muscle cells, enclosed in a pseudocapsule as it compressed the adjacent normal smooth muscle tissues. Grossly, it is a nodule which can be located as described :

·         Adjacent to and bulging into the endometrial cavity (submucous fibroid)

·         Centrally within myometrium (intramural fibroid)

·         Outer border of the myometrium (subserosal fibroid)

·         Attached to uterus by a narrow pedicle containing blood vessels (peduculated fibroid)

It is believed to be an estrogen-dependant mass. Fibroids have higherer concentrations of estrogen receptors if to be compared with normal myometrium. Hence, estrogen plays a major role in setting the pathogenesis of fibroids in motion. This is evidenced by increasing prevalence during reproductive ages particularly more than 30 yrs old and markedly reduce following menopause. It is never present in preadolescent female.

Early menarche and obesity also are associated with risk of developing fibroid due to exposure towards endogenous steroid hormones. Having family history of fibroids and nulliparity do increase the risk as well. Caution is required, however, when linking association to cause.

Fibroid is often asymptomatic,requiring no treatment or may also be found coincidentally. Patients may presented with prolonged history of menorrhagia together with remarkable anemia symptoms made her decided to bring the medical problem to attention of physician. 

Menorrhagia by definition, is an excessive menstrual bleeding diagnosed when monthly menstrual loss exceeds 80ml. It  usually signify that the fibroid is of submucous origin because it increases the endometrial surface area hence distorting the endometrial cavity. There are other possible symptoms which might occur in women with fibroid such as :

• ·         Subfertility as it distorts the endometrial cavity, preventing the implantation of a fertilized ovum. Fallopian tube might be occluded as well.
• ·         Compressive symptoms if it is large enough to compress the adjacent organs such as rectum and urinary bladder, causing tenesmus and increased urinary frequency respectively.
• ·         Pain if there is acute degeneration of the tissue. This is often associated with mild pyrexia and leuckocytosis.
• ·         Pregnancy problem such as abnormal lie and postpartum hemorrhage secondary to inefficient uterine contraction.

There was a patient, I've clerked for my case write up, let say Madam Lola... in her case she denied denied any pressure symptoms like urinary retention or frequency, constipation or tenesmus. She is also fertile and never had problem with her pregnancy except for her miscarriage in second pregnancy. The cause of the miscarriage was unknown, as that happened 19 years ago so the patient couldn't recall why she had the miscarrriage. However, endometrial pathology may cause miscarriage as mentioned before. There was no pain in case of the Madam Lola.

After the fibroid is suspected based on the history (e.g.: heavy menses, lethargy) and general inspection (eg: pallor), evaluation usually started with pelvic examination which includes both speculum examination and bimanual examination. Abdomen should be examined thoroughly to describe the mass, hence helps in narrowing the diagnosis. Full blood count which is routinely done is very important to confirm the anaemia.

Transvaginal ultrasound is often done to confirm the source of a pelvic mass and define the anatomy of pathology which can lead to menorrhagia like what Puan Farida have had. Hysteroscope is best carried out to see the uterine cavity, at which sometimes is helpful in obtaining endometrium sample for histological analysis.

Management and treatment of choice involves counselling of the patient by the specialist beforehand, considering the desire of the patient (and the spouse if married) whether they have desire to keep the patient’s fertility, socio-economical status and cosmetic purpose.

Treatment options are :

a)      Conservative management

·         In asymptomatic and minimal symptom

·         Follow-up for 6-12 monthly to asses the growth rate by abdominal examination and ultrasound

b)      Medical management

·         Gonadotrophin-releasing hormone to shrink (reduce vascularity and size) the fibroids. It can be used to reduce the size prior to surgery if necessary. This is useful in reducing blood loss and transfusion.

c)      Surgical management

·         Myomectomy : preferred if fertility is desired but more risk of threatening bleeding which may be proceeded with emergency hysterectomy.

·         Hysterectomy  :  The definitive of treatment for menorrhagia. There are several types of hysterectomy, distinguished by the method used to approach the organ.

·         Hysteroscopic resection

·         Embolization of uterine artery : latest option peformed by interventional radiologist.

Vaginal hysterectomy was a treatment of choice for Madam Lola and agreed by her husband because they do not have plan to have any more children in the future. She also would prefer to avoid scar left on her abdomen to have a better quality of life after the surgery.

           

Btw, nowadays, it is not really accurate to describe heavy menstruation  as menorrhagia. Most specialists I've   met they prefered to describe the heavy menstruation  in detailed manner and don't  prefer to use the term menorrhagia. Whether it is prolonged, regular, increased number of pads...etc. 

 In obstetric, fibroid may interfere with normal fetal lie as well. And fibroid degeneration ia quite common as well, leading to acute abdominal  pain in pregnancy. Chack that out. 

References

Voorhis, B. V. (2009) A 41-Year-Old woman with menorrhagia, anemia, and fibroids: review of      

          treatment of uterine fibroids, JAMA, 301(1):82-93

Monga, A., Dobbs, S. (2011)  Gynaecology by ten teachers. CPC Press.

 Shaw, H. A. (2013, June 5). Vaginal Hysterectomy  [Article for reference]. Retrieved 2014,   

         September 23 from http://emedicine.medscape.com/article/1839938-overview.