- 9:47:00 PM
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MY SLIDESHARE
- 12:57:00 AM
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PEDIATRIC SURGICAL PROBLEM :
INTESTINAL MALROTATION WITH MIDGUT VOLVULUS
INTESTINAL MALROTATION WITH MIDGUT VOLVULUS
NORMAL EMBRYOLOGICAL ROTATION OF THE MIDGUT
Definition
Intestinal malrotation is a congenital anomaly that results when the normal sequence of rotation and fixation of the bowel fails. Midgut volvulus is a complication of malrotation when the bowel twists around a fixed point usually mesentery that has adhesed to the bowel causing obstruction (see Figure 4).
FIGURE 4
Epidemiology
Malrotation is uncommon, and its prevalence in children younger than 1 year of age is 3.9/10,000 live births; however, it can lead to irreversible intestinal necrosis, which can be fatal, and so one must have a high index of suspicion to make the diagnosis.
Most children present within the first month of age and the majority within the first year of life. Morbidity and mortality largely depend on the extent of bowel ischemia, which has been largely attributed to a delay in diagnosis.
Males are slightly more affected than females (2:1).
Pathophysiology
During normal embryologic development a counterclockwise turn of both the proximal and midgut portions of the intestine occurs around the fourth to tenth week of gestation, prior to the intestine retracting into the abdomen.
Abnormalities of rotation physiology result in excessive mobility and compression of the bowel, leading to twisting or volvulus.
Mesentery can stick to the bowel and act as a fixed point that the intestine can rotate around, or the bowel may not be fixated correctly to the posterior abdominal wall, which allows the whole midgut to lie free within the abdomen.
Any part of the intestine may twist and become obstructed, resulting in midgut, cecal, or duodenal volvulus.
Clinical Features
Classically, malrotation with obstruction presents with bilious vomiting, but overall presentation varies.
Bilious emesis indicates obstruction below the ampulla of Vater, which is a common place for obstruction to occur in the setting of malrotation; although bilious emesis is not pathognomonic for volvulus, it is important to emphasize midgut volvulus should be highly considered in the neonate presenting with bilious emesis.
The age of the infant affects appearance of disease. Neonates may be fussy and parents may complain of feeding difficulties, intermittent apnea, or even failure to thrive. Older infants may appear to have abdominal pain and diarrhea with or without hematochezia and vomiting. Physical exam findings are non-specific; peritoneal signs indicative of perforation that can lead to sepsis and shock are late signs and indicate a poor prognosis.
Diagnostic Studies
The diagnostic studies performed largely depend on the clinical appearance of the child. A broad net with respect to testing is needed in the toxic-appearing infant. Upper gastrointestinal (UGI) contrast study to assess the third and fourth part of the duodenum is the gold standard to make the diagnosis.
A classic “corkscrew” appearance in the volvulus can be identified with sensitivity of 96%.
Figure 5 shows the X-ray of a newborn presenting with bilious vomiting. The flat and decubitus X-ray shows asymmetry of the bowel gas with distended loops of bowel in the right side and left side of the abdomen. This patient had malrotation with midgut volvulus.
Figure 5. Decubitus (A) of Neonate with Midgut Volvulus
Asymmetry of the bowel gas with a moderately distended loop of bowel in the right and left side of the abdomen. This newborn has midgut volvulus. A Decubitus view
Figure 5. X-ray flat (B) of Neonate with Midgut Volvulus
Asymmetry of the bowel gas with a moderately distended loop of bowel in the right and left side of the abdomen. This newborn has midgut volvulus. B Flat view
Figure 6 is an upper gastrointestinal study depicting midgut volvulus in a newborn; the study shows that the duodenal jejunal junction crossed to the left of midline but did not extend superiorly as expected, and there was no peristalsis identified within the stomach or duodenum.
Figure 6. Upper Gastrointestinal Study Depicting Midgut Volvulus in a Newborn
The duodenal jejunal junction crossed to the left of midline but did not extend superiorly as expected, and there was no peristalsis identified within the stomach or duodenum.
Ultrasound of the mesenteric vessels can also be obtained looking for a “whirlpool sign,” which is a swirling shape seen when the superior mesenteric vein (SMV) and mesentery encompass the superior mesenteric artery (SMA), or for “reversal sign.”
Figure 7 is an ultrasound showing SMV/SMA reversal sign in midgut volvulus. The sensitivity and specificity of ultrasound are slightly lower than UGI contrast studies, and, as such, ultrasound usually is used as an adjunct.
Figure 7. Ultrasound Showing SMV/SMA Reversal Sign in Midgut Volvulus
Unstable neonates with sepsis, severe metabolic acidosis, or systemic shock presenting with bilious emesis and abdominal distension should likely forgo imaging and proceed with surgical exploration. CT scanning is not routinely performed unless the child’s presentation is ambiguous or an alternative pathology, such as intra-abdominal mass, is high in the differential.
Differential Diagnosis
The differential diagnosis for malrotation largely depends on the age of the child, although many will present with abdominal pain. Malrotation volvulus usually presents in children younger than 1 month of age, so the differential diagnosis will include illnesses more common in this age group. However, one should suspect malrotation midgut volvulus in a child of any age presenting with bilious vomiting and abdominal pain.
Necrotizing enterocolitis should be considered if the child is premature and presents with changes in feeding and abdominal distention.
Older infants presenting with signs of intestinal obstruction and altered mental status should raise concern for intussusception.
Pyloric stenosis can present with vomiting; however, vomiting is always non-bilious. It is important to note that malrotation volvulus can present in children of any age and has been diagnosed in adults as well.
Management
Malrotation volvulus is a surgical emergency and requires a laparotomy. Intravenous access should be obtained promptly and aggressive fluid resuscitation started. Nasogastric tube should be placed and antibiotics initiated to cover gram-positive, gram-negative, and anaerobes.
Immediate surgical consultation, perhaps even prior to obtaining imaging, may be indicated if the patient is unstable and malrotation volvulus suspected. Morbidity and mortality increase if the obstruction is not treated within 24 hours.
Surgery is performed to correct the obstruction and minimize risk of future volvulus; the surgery will not correct the actual malpositioning of the bowel. The surgical approach, laparotomy or laparoscopic, does not affect length of stay or the complication rate.
If bowel necrosis is found, bowel resection will occur, placing the patient at risk for short bowel syndrome, again, emphasizing the need for prompt diagnosis and treatment. The longer the bowel stays obstructed the more likely ischemia and necrosis ensue.
Disposition
Children diagnosed with malrotation volvulus require admission at a facility with pediatric surgical resources. Transfer should be considered even prior to diagnosis if malrotation volvulus is suspected.
Summary
Intussusception is usually diagnosed in children younger than 2 years of age. It affects males slightly more often than females. The exact etiology is unclear; however, there is an association with gastroenteritis and viral syndromes such as upper respiratory tract infection, otitis media, and influenza. Most frequently, the intussusception occurs between the ileum and the colon. Children can present with intermittent abdominal pain, vomiting, and currant jelly or red stools; however, the latter is a late sign. Intussusception should be considered in a child presenting with altered mental status. Non-invasive radiological reduction should be attempted; however, if the child appears critically ill, pediatric surgery should be consulted promptly.
Malrotation midgut volvulus most commonly presents in children younger than 1 month of age. Bilious emesis in a neonate should be considered a surgical emergency until proven otherwise. Patients can present with irritability, feeding difficulties, failure to thrive, and abdominal pain. The diagnosis can be challenging and delays in diagnosis increase morbidity and mortality significantly. Signs of bowel ischemia, such as hematochezia or sepsis, indicate a poor prognosis. UGI contrast study is the gold standard diagnostic modality, and pediatric surgical consultation is required since an operation is required.
Overall, children presenting to the ED with abdominal pain can be challenging to diagnose. ED physicians are charged to differentiate between self-limited pathology and more life-threatening surgical emergencies. Intussusception and malrotation midgut volvulus both can present with abdominal pain, vomiting, and irritability. Both can be fatal if the diagnosis is delayed or missed, and so one must have a high index of suspicion.
REFERENCE :
RELIAS FORMERLY AHC MEDIA , Intussusception and Midgut Volvulus. June 2015.
[https://www.ahcmedia.com/articles/135491-intussusception-and-midgut-volvulus]
- 12:30:00 AM
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notes:
This is not my own link. I copy and paste it here from a websites called HOUSE OFFICER WORKSHOP MALAYSIA to share with you all. You can directly go to the websites and download other books here.
- 8:33:00 PM
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notes:
This is not my own link. I copy and paste it here from a websites called HOUSE OFFICER WORKSHOP MALAYSIA to share with you all. You can directly go to the websites and download other books here.
- 8:30:00 PM
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Hope this helps to guide you through the course somehow. I find it quite useful and helps me a lot during my posting as a medical student in the hospital.
notes:
This is not my own link. I copy and paste it here from a websites called HOUSE OFFICER WORKSHOP MALAYSIA to share with you all. You can directly go to the websites and download other books here.
- 8:28:00 PM
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Orthopaedic is the branch of surgery concerned with conditions involving the musculoskeletal system. Orthopedic surgeons use both surgical and nonsurgical means to treat musculoskeletal trauma, spine diseases, sports injuries, degenerative diseases, infections, tumors, and congenital disorders.
This is a useful book for your guidance in this posting. It helps me and my friends a lot.
notes:
This is not my own link. I copy and paste it here from a websites called HOUSE OFFICER WORKSHOP MALAYSIA to share with you all. You can directly go to the websites and download other books here.
- 8:24:00 PM
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POST END POSTING EXAM - LONG CASE
Fuhhh, I just told you guys that I don't want stroke patient this morning right? Turn out I went to see my patient and suddenly my patient that I got is a stroke patient. WOW. What a case... I almost broke into tears and I became very nervous. Thank God, Liyana was there helping me out to prepare for the case. She did all the research while I try to memorise and smoothing my CNS physical examination flows.
Nina was there too and helping me out with the physical examination. I'm blessed to have friends like them. My subgroup-mates also very supportive and wish me luck with the patient.
I went to Mahsuri ward at 2.00 pm and starting to clerk the patient. Then I receive a message from Dr. Ong that I need to clerk Bed 15 instead Bed 2. I asked her for confirmation, and she said Bed 15 for me. Mann..
I called my friend and I told her our case had been swapped - giving her hints that she need to read about CNS examination and ischaemic stroke 2ry to cardioembolism instead CVS case.
He came due to left upper and lower limb muscle weakness.
My case - The CVS patient
The CNS CASE
The patient was a 65 year old malay gentleman but seems old from his age. He has underlying Chronic Rheumatoid Heart Disease, Chronic Kidney Disease and Gouty Arthritis.He came due to left upper and lower limb muscle weakness.
My case - The CVS patient
My patient was well cooperate and very friendly. 1 hour was not enough for me to clerk and did my examination (suprisingly!). 1 hour given to me was always enough before this, I wonder if changing my style by first listening to all the patient had to say is better than while listening I should jotted down everything and arrange it all together. Hmm. The latter seems better for me.
My patient was a 43 year old, malay gentleman working as hawker and live in Melor, Kota Bharu. He is a smoker with history of 21 pack years for more than 30 years. He stopped smoking last month.
Patient is a known case of hypertension and also hypercholesterolnemia. He was diagnose with hypertension since 2 years ago and not compliance to medication. His hypercholesterolnemia was diagnosed last month and claimed compliance to medication.
His main complaint was chest discomfort, breathlessness and lethargy. Then nothing. Aiyoo. There was 5 days history admission to CCU recently (last month) due to almost similar presentation but worsen than the current one. He was not aware of the diagnosis. But listening to his description about the symptoms is more likely like acute myocardial infarction or acute heart failure.
Upon physical examination, Apex beat was not displace (5th intercostal space, mid-clavicular line), there was thrills present at left sternal edge. Pansystolic murmur was heard best heard by diaphragm at mitral area and radiated to axilla - bloody hell it was mitral regurgitation! And I was so pleased with myself that I can finally differentiate the type of murmur. Bibasal crepitation was heard and there was no sacral and pedal edema.
My differential diagnosis were Acute Coronory Syndrome and also Heart Failure. Dr. Ong asked me about the investigation I would done and management for Acute Coronary Syndrome Disease. She gave me good mark, Alhamdullilah !
Investigation I would carry out :
1) FBC - looking for any infections from total white count and looking for anemia from Hb level.
2) Coagulation Test
3) Renal profiles
4) Liver Function Test
5) Cardiac Biomarkers - Troponin & CKMB
6) ECG - ST elevation in Myocardial Infarction
7) Chest X-Ray - to look for any cardiomegaly or other underlying disease
8) Echocardiogram - To see the LVEF status, cardiac wall, cardiac contractility and to confirm mitral regurgitation
Management:
1) Airway
2) Breathing
3) Circulation
4) Give oxygen if patient still breathlessness
5) Primary PCI
6) Anti-fibrinolytic such as streptokinase or ateplase
7) Anti hypertensive drug - Frusemide
8) Educate patient
💕 READ HOW TO DIFFERENTIATE MURMURS 💕
HERE
- 6:55:00 PM
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Long case exam is just in few hours from now and I'm so nervous about it. What if I got stroke patient? OMGG me,myself will be having stroke in front of the patient. I hope Dr. Ong will give me a straightforward case and I'm able to tackle that case too, in shaa Allah. Ease all my journey today ya Rabb.
So last night I was revising about CVS examination and got confused all over the topics. Like, WTH am I reading for the past 1 hour then got forgot again. Allahu my brain... *sigh*
Having difficulty in differentiating type of murmurs while auscultate a patient? Don't worry, you're not the only one ! Me too having the same problem since I was a 3rd year medical student. During that time, I was at Hospital Tanah Merah and I did not came across any patient with murmur. Cases were limited as it is a district hospital. All severe cases will be referred to Hospital Kota Bharu. So, I'm here now in Kota Bharu as a 4th year medical student. So many patient with interesting physical findings and most of them have murmur! YAY.
So here some tips I learnt from my prof and also from hospital specialist. One of my prof blog about it - A Simplified Approach to Cardiac Murmurs For Medical Students. And it is very helpful for me and makes my life easier. A bit confused in beginning but later you'll be okay.
From the blog:
The basic principles are:
- if the murmur coincides with the first heart sound, it is a systolic murmur.
- If it doesn't coincide with the first heart sound, it is a diastolic murmur.
Sometimes, even if you have done your best and listened while palpating the pulse, and you are still not sure whether it is a systolic or diastolic murmur, well, in the exams, you can guess and you have a fifty-fifty chance of getting it right (or wrong).
If you had to guess, then go for systolic murmurs as they tend to be:
- more common
- easier to hear compared to diastolic murmurs which tend to be low-pitched
Of course when guessing, there is a chance one might be wrong. Rather have no answer, sometimes it is better to guess.
For the sake of simplification, I memorised, as a medical student, four of the more common murmurs:
- Mitral regurgitation
- Aortic stenosis
- Mitral stenosis
- Aortic regurgitation
Here the best part about my prof. She summarised it all like this:
Mitral regurgitation is a pansystolic murmur that is heard loudest at the apex, heard through out the praecordium, radiates to the axilla, and is accentuated by expiration.
Aortic stenosis is an ejection systolic murmur heard loudest at the aortic area, radiates to the carotids, and in accentuated by the patient leaning forward in expiration.
Mitral stenosis is a mid-diastolic rumbling murmur heard at the apex and accentuated with the patient leaning on the left side in expiration.
Aortic regurgitation is an early-diastolic murmur heard best at the left sternal edge/tricuspid area, accentuated by the patient leaning forward in expiration.
Aortic stenosis is an ejection systolic murmur heard loudest at the aortic area, radiates to the carotids, and in accentuated by the patient leaning forward in expiration.
Mitral stenosis is a mid-diastolic rumbling murmur heard at the apex and accentuated with the patient leaning on the left side in expiration.
Aortic regurgitation is an early-diastolic murmur heard best at the left sternal edge/tricuspid area, accentuated by the patient leaning forward in expiration.
Here some video that might help you to differentiate between those murmurs
MITRAL REGURGITATION
AORTIC STENOSIS
MITRAL STENOSIS
AORTIC REGURGITATION
- 10:03:00 AM
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Cushing’s Triad is a clinical triad described with bradycardia, Systolic hypertension and irregular breathing. It is named after Harvey William’s Cushing, who actually demonstrated Cushing's reflex (again him) first.
Cushing’s Reflex is the physiological phenomena, in which raised intracranial pressure leads to irregular breathing, bradycardia and systolic hypertension/ increased wide pulse pressure. Cushing’s Reflex is also known as Cushing’s Effect, Cushing’s Reaction, Cushing’s Phenomenon and Cushing’s Law.
MECHANISM
The Cushing reflex is complex and seemingly paradoxical. The reflex begins when some event causes increased intracranial pressure (ICP). Since the cerebrospinal fluid is located in an area surrounded by the skull, increased ICP consequently increases the pressure in the fluid itself. The pressure in the cerebral spinal fluid eventually rises to the point that it meets and gradually exceeds the mean arterial blood pressure (MABP or MAP). When the ICP exceeds the MABP, arterioles located in the brain's cerebrum become compressed. Compression then results in diminished blood supply to the brain, a condition known as cerebral ischemia.
During the increase in ICP, both the sympathetic nervous system and the parasympathetic nervous system are activated. In the first stage of the reflex, sympathetic nervous system stimulation is much greater than parasympathetic stimulation. The sympathetic response activates alpha-1 adrenergic receptors, causing constriction of the body's arteries. This constriction raises the total resistance of blood flow, elevating blood pressure to high levels, which is known as hypertension. The body's induced hypertension is an attempt to restore blood flow to the ischemic brain. Sympathetic stimulation also increases the rate of heart contractions and cardiac output. Increased heart rate is also known as tachycardia. This combined with hypertension is the first stage of the Cushing reflex.
Meanwhile, baroreceptors in the aortic arch detect the increase in blood pressure and trigger a parasympathetic response via the vagus nerve. This induces bradycardia, or slowed heart rate, and signifies the second stage of the reflex.[Bradycardia may also be caused by increased ICP due to direct mechanical distortion of the vagus nerve and subsequent parasympathetic response. Furthermore, this reflexive increase in parasympathetic activity is thought to contribute to the formation of Cushing ulcers in the stomach, due to uncontrolled activation of the parietal cells. The blood pressure can be expected to remain higher than the pressure of the raised cerebral spinal fluid to continue to allow blood to flow to the brain. The pressure rises to the point where it overcomes the resisting pressure of the compressed artery, and blood is allowed through, providing oxygen to the hypoxic area of the brain. If the increase in blood pressure is not sufficient to compensate for the compression on the artery, infarction occurs.
Raised ICP, tachycardia, or some other endogenous stimulus can result in distortion and/or increased pressure on the brainstem. Since the brainstem controls involuntary breathing, changes in its homeostasis often result in irregular respiratory pattern and/or apnea. This is the third and final stage of the reflex.
Commonly, in various pressor reflexes, the central chemoreceptors, which transform chemical signals into action potentials, and the baroreceptors, which sense pressure changes of the carotid sinuses, work together to increase or decrease blood pressure. However, chemoreceptors do not play a role in the Cushing reflex. Thus, even in the presence of sympathetic stimulation from the brain, which would normally produce tachycardia, there is in fact bradycardia.
FUNCTION
Raised intracranial pressure can ultimately result in the shifting or crushing of brain tissue, which is detrimental to the physiological well being of patients. As a result, the Cushing reflex is a last-ditch effort by the body to maintain homeostasis in the brain. It is widely accepted that the Cushing reflex acts as a baroreflex, or homeostatic mechanism for the maintenance of blood pressure, in the cranial region.
Specifically, the reflex mechanism can maintain normal cerebral blood flow and pressure under stressful situations such as ischemia or subarachnoid haemorrhages. A case report of a patient who underwent a spontaneous subarachnoid haemorrhage demonstrated that the Cushing reflex played a part in maintaining cerebral perfusion pressure (CPP) and cerebral blood flow. Eventually, the ICP drops to a level range where a state of induced hypertension in the form of the Cushing reflex is no longer required. The Cushing reflex was then aborted, and CPP was maintained. It has also been shown that an increase in mean arterial pressure due to hypertension, characteristic of the reflex, can cause the normalization of CPP. This effect is protective, especially during increased intracranial pressure, which creates a drop in CPP.
REFERENCE:
- 11:52:00 PM
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Hi guys, I'm a 4th year medical student from Lincoln University College. Currently in Internal Medicine posting for 4 weeks. This is my second week in this posting and gotta share what I learnt last week.
Four groups has been assigned to four different Medicine wards in Hospital Raja Perempuan Zainab (HRPZ) II; Mahsuri, Bendahara, ward 8/8P and also Puteri. My first week is at Ward Mahsuri.
Then, Dr. Azza gave us a list of specialist in charged for each group. My group was assigned to few specialist there, including Dr. Sinari. She is the consultant of Medicine department. Our favourite specialist for time being is Dr. Grace from Mahsuri ward. She is so nice, graceful and very knowledgeable. She treat her medical officer and houseman so nice that I felt lucky to have her as one of our group specialist in-charged. Bless us. Bless me.
First day was tiring but there was no bed side teaching. Second day of first week, we went to the ward and introduce ourself to the staffs there. Most of the houseman there are very nice. They include us in every ward round and help us whenever we look blur in the cubicle. The medical officer in charged for cubicle 3 in ward Mahsuri is Dr. Mohd. He is the coolest person there. I mean, as a medical officer, he really concern about the patient and also the houseman under him. Those houseman under him and Dr. Grace were lucky. Other medical officer in the ward that I find very amusing is Dr. Hidayah. She is so rock and cool. She got this mighty confident and a very unique lady, I must say.
During ward round, Dr. Grace will include us in the discussion as well. She ask questions and also explain about the case, the decision-making, and also the insight of that case. Dr. Mohd also help us and discuss the case briefly so that we understand the case well when the ward round take place. For the first time, I felt like being welcomed by the specialist, medical officer and also all the staffs there. They are too nice. I can't believe that I'm in medicine posting.
We were given homework at the end of ward round. For me, it is more like a reading list or list of topics that you need to read at home. So here are the list for the 1st week of posting:
1. Hypertensive Intracranial Bleeding 👌
2. Atypical Pneumonia 👌
3. Community Acquired Pneumonia 👌
4. Retroviral Disease 👌
5. Upper GI Bleed
6. Status Epilepticus
👌 = DONE
Till now, I haven't touch those last two topics. Hahaha. Sigh. Then we went for a clinic session. First clinic session was a rheumatology clinic. But we were some sort of not welcomed and kena marah in front of the patient inside the doctor's room. I almost cry but kinda tahan because the fault was not from our side. We did all the things that we need to do; we introduce ourself at the counter. We ask who in-charged for the clinic. We introduce ourself again to the nurses in the doctor's clinic and asked for permission. The person in-charged was not there so we waited outside. Suddenly the nurse came to us and informed us that we can asked for permission from the doctors in the other room. So we all went inside the room and again, introduce ourself to the two medical officers inside that tiny room. It was so crowded. One of the doctor told us to clerk a patient who is currently waiting outside the room. So yeaa. We clerked. We followed the patient went inside meeting other medical officer. And then after everything almost end, a lady came inside the room and marah us for not introducing ourself. We were so puzzled that time as we already did the introduction part and still kena marah. We explained and she was like still perli us about not respecting the clinics. They were not informed yada yada. Sigh. Sometime you buat everything also kena marah. So yeaaa whatever.
Another clinic experience is with Dr. Pong from Respiratory Clinic. She was so nice, so cute, so cool and so friendly with the patient, including us. We sit inside the room and she will ask questions related to each patient that came to see her. We felt like we were welcomed and she teaches us about pulmonary fibrosis that day.
Here are my second week posting reading list:
1. Cushing reflex 👌
2. Renal with hepato involvement
3. Typhoid Fever
4. Pott's Disease
5. Liver Cirrhosis
6. Obstructive Jaundice
7. Upper GI Bleed
8. Status Epilepticus
Date: 18 March 2018
1. Hypergylcemic Hyperosmolar State (HHS) 👌
2. Hypoventilation Obesity Syndrome
3. Cardiomyopathy 👌
4. Uremia
5. Delirium vs Dementia
6. Congestive Heart Failure 👌
7. Upper GI Bleed
8. CVS Murmur Maneuvers 👌
Date: 19 March 2018
1. Asthma / COPD
2. Respiratory Failure
3. CNS Examination
4. Causes of stroke
👌 = DONE
So many things to cover right ?
- 10:56:00 PM
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Growing up with siblings of doctors, my dad always advised us with an important advice, so profound that I remember it till today.
" Medical is a world of silent bragging. Everyone brags. From housemen to consultants. Just remember to keep yourself rooted. Always."
I've worked for almost 6 years. And I have to say, you are right Dad. Very very right.
Everyone brags in this field. Some doctors brag about their qualifications. Others brag about their experience.
Some brags about their management. Others brags about their skills.
Some mo think the ho don't deserve to become doctors. But they forget the fact they become mo is because they just happen to finish housemanship earlier. Not because they are more qualified.
Some specialists look down down on other doctors. They forget that passing your exam early doesn't mean you are more qualified as a specialist. Failing exam and passing late doesn't mean you are less qualified.
Consultants look down on specialists.
Specialists look down on mo.
Mo look down on ho.
Senior ho look down on junior ho.
Ho look down on nurses.
Clinicians look down on non clinicians.
Big hospitals look down on district hospitals.
Hospitals look down on KK.
It never stops!
How do we respond to those who brag?
My dad's way is simple :
" If people brag. Let them be. Its their way of boosting up their falling self esteem. Confident people dont brag. They dont need to put people down to feel good about themselves. So if these people brag, just feel sorry for them. But if they belittle you, speak up!"
Trust me.
It. Works.
Everytime!
Ps : tak perlulah rasa diri hebat. Masuk kubur kena jadi makanan cacing jugak.....
HO - Houseman
MO - Medical Officer
KK - Klinik Kesihatan
- 6:02:00 PM
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HISTORY TAKING TEMPLATE
So I'm gonna share with you gaisss my template for clerking patient. Well, this is just a basic thing that you need to ask when you clerk a patient. In paediatric ward, you can't really take genuine history from the child. I mean, how you're gonna take history from a child right? They might be crying so loud that even the parent would thought you're an incompetent doctor at that time. Haaaa, so take history from the parent, NOT from their grandmother, their uncles, their sibling (depend on situation) or other unrelated people who came with the patient. Preferably take history from the mother. Mother know the best! They can provide all information you wanted to know.
There are 2 templates that I did for my study purpose.
- For template A, I put few things from Geeky Medic. Reference source is from Geeky Medic.
- As for template B, I re-edited it and followed a bit like Hospital Raja Perempuan Zainab (HRPZ) II history template. Reference source is from Geeky Medic.
Template A View
Template B View
Please don't claimed this as your own, and do not re-upload or share it without permission. Thank you !
1. TEMPLATE A
2. TEMPLATE B
- 9:16:00 PM
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by PUTREEO
Liyana and Audi already settle with their make up, so we all headed to Kamdar Textiles in the heart of Kota Bharu city. Why Kamdar? because you can get saree at a cheaper price there and the salesgirl will help you wear saree with free of charge. But if you're outsider (not purchasing Kamdar's saree but you're just want the service of salesgirl tolong pakaikan your saree) they charged RM 10/person. Okay-lah.
Meet Liyana Mikayla. Ni la anak Umaira and Azim. Budak kecik comel yang menghiburkan my batch last night.
- 12:22:00 PM
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