Words shall not describe what I bring away from TIHTC and my gratitude for it all...

I look back...

Week 1: Oncology
Day 1: Internal medicine meeting, out patient clinic, in-patient rounds
Day 2: Internal medicine meeting, out patient clinic, colorectal cancer presentation, target therapy presentation
Day 3: Internal medicine meeting, TIHTC orientation, introduction to pathology equipments and protocol, patient interview
Day 4: Internal medicine meeting, Pathology review of Colon Cancer section, Acupuncture for Chemo-induced nausea and vomiting, Neurology case conference

Week 2: Cardiology/ Cardiovascular surgery
Day 1: Internal medicine meeting, outpatient clinic, inpatient rounds, EKG, pacemaker removal operation/ infected wound cleaning
Day 2: Surgical department meeting, echocardiography, abdominal ultrasound, exercise stress test protocol, EKG, evening outpatient clinic
Day 3: Double lead pacemaker placement, dialysis AV shunt balloon angioplasty, AV graft thrombectomy
Day 4: Introduction to extra-corporeal membranous oxgenator, surgical department conference, Out patient clinic, in-patient rounds
Day 5: Observe stent placement to repair abdominal aortic aneurysm

Week 3: Neurosurgery
Day 1: Finalize group colorectal cancer case presentation with Dr. Chen, visit ICU, introduction to intracranial shunts and ICP monitoring
Day 2: Surgical department meeting, observe C4/C5 disc herniation, disc removal, spinal nerve decompression and prosthetic disc insertion, brain CT discussion Tentorial subdural hemorrhage: differential diagnosis and complications, evening outpatient Clinic with Dr. Chen
Day 3: Tracheo tube removal, discussion of emergent decompressive craniotomy to remove the hematoma, patient chart review, continuous ICP monitoring, lunch time documentary on Herceptin, observe L3/L4 decompression surgery
Day 4: Introduction to trauma neurology: diagnosis, signs, symptoms, and treatment protocol, goals
Day 5: Introduction to cervical ultrasound, intracranial circulation, and economics of private neurosurgery

Week 4: Nephrology
Day 1: Pediatrics meeting, introduction to hemodialysis and protocol, inpatient rounds, interpret imaging studies and lab values (chemistry panel)
Day 2: Internal medicine meeting, out patient clinic, inpatient rounds
Day 3: Internal medicine meeting, admission H&P for recurrent pyelonephritis patient
Day 4: Visit Shenkeng Public Health Center
Day 5: Observe consult with vegetative patient’s family on ventilator removal, epidemiology research data collection, inpatient rounds, observe femoral double shunt placement for emergent dialysis

I remember...

1. Dr. Chin Yi Chen was the preceptor for 3 of us during the first week. He taught us many things in the short 4 days we had. In addition to outpatient clinic and inpatient ward rounds, he presented powerpoint on numerous topics including target therapy, colorectal cancer, case studies, Chinese medicine, and individualized genetic cancer treatment. He also encouraged us to interview patients and learn about their disease and treatment course. Dr. Chen was extremely good at patient education—he was able to tell the patient a story of his/her illness in such a way that patient understand and comply with the medical recommendation he made. Many of his patients emphasized that he was the best doctor in their personal experiences. For the following 3 weeks, Dr. Chen also allowed us to shadow him in his Tuesday evening outpatient clinic. His assistance and guidance went way beyond his duty as our preceptor; he even spent an entire morning to help us re-structure, collect data, and refine our case study presentation on colorectal cancer.

2. I attended various morning departmental meetings: internal medicine, surgery, and pediatrics. These were fantastic ways to start a day. During one hour, one to 15 or 20 cases were presented and discussed. I enjoyed the fast pace and interactive discussion, very conducive to knowledge expansion and application. The pediatric chief and Dr. Wu from internal medicine were especially encouraging and accommodating. They would often emphasize differential diagnosis and pathophysiology principles.

3. Cardiology and cardiovascular surgery worked seamlessly together. Learning from both specialties in one week was an incredibly exciting and productive experience. Dr. Kuei-Feng Chen showed us the breadth and depth of cardiology; he also exemplified high standards for patient care and professionalism. As the director of Cardiology, he led an outstanding team of dedicated physicians such as Dr. Yu (young attending) and Dr. Fong. As I observed (in lead suits myself) Dr. Yu place a double lead pacemaker in a 90-year-old patient, I realized that cardiology is not for the faint of heart. The CV surgeon was also enthusiastic about teaching, welcoming Sandy and I to observe numerous operations (AAA stent repair, AV shunt thrombectomy) even though he was Nicole’s preceptor.

4. I appreciate the multi-faceted learning experience our preceptors/ TIHTC staff structured for us. I was able to observe and learn from numerous surgeries, patient/ family consultation, outpatient clinic, inpatient ward rounds, departmental meetings, case conferences, imagining studies and interpretation, and develop my own research project. I can hardly imagine a more fruitful and meaningful experience than these 4 weeks.

5. Dr. Yi Gian Chen (Chief nephrologist) and Dr. Shui are amazing teachers. Not only do they teach me a lot about chronic renal diseases and hemodialysis, they also support and guide my intellectual quests in every possible way. I discuss my idea of doing epidemiologic research on end stage renal disease patients with Dr. Chen. He listens to my proposal patiently and helps me collect as much data as possible. He generously shares his experience and knowledge of current research and trends, assisting me to refine my research goals and methods. He even mentioned the opportunity to collaborate with 3rd year resident on future research!

6. Dr. Ding, one of the neurosurgeons at Taipei hospital, gave me the opportunity to assist in spinal surgeries as the first assistant. This was an eye-opening experience and great honor. He also guided us through a complex and interesting discussion of cerebral hemorrhage. He shared about his current pursuit of PhD in Healthcare Queue Management. He explained one project he was working on: how to maximize the utility of emergency beds a hospital maintain. I thoroughly enjoy the richness and multi-dimensions of medicine, from concrete intricate surgeries to abstract mathematic modeling.

7. I really liked Dr. Liao’s powerpoint presentation on trauma neurology. I learned a lot of information; the actual cases he shared were very helpful in solidifying major patho-physiologic principles and treatment protocol.

I would have done this again because TIHTC

1. Solidify and expand the knowledge I have obtained from my first year of pre-clinical studies at Touro University.

2. Rotations such as neuro-surgery served as good preview of selected topics in my second year studies.

3. Prepare me for 3rd and 4th year clinical rotations.

4. Show me ways to improve health care in US. Real time electronic medical records optimize healthcare delivery efficiency and streamline information flow among departments.

5. Taiwanese doctors see their patients as whole persons, not discrete organs of interest or disease states. I witness that even highly specialized physicians such as oncologists, nephrologists, and cardiologists share a holistic approach to patients. This resonates deeply with The Principles of Osteopathy.

6. One of the most meaningful and productive ways to spend the only summer vacation I have in the years to come. My passion for medicine was renewed; my mind challenged and my heart inspired.

World travel of the human body--kidney, liver, heart, brain back to kidney!

7-8am, 9-12pm—extremely interesting nephrology case and ward rounds

Dr. Chen (chief nephrologist) told me yesterday about a complex and interesting case yesterday Dr. Shiu briefed me on the case and showed me how to access electronic medical records for the patients. He said that I could go to the hospital at anytime to study the patient’s records. I was so excited and felt very privileged. Because our group celebrated and had lots of fun at Shuling night market last night, I rose early this morning and headed to the hospital to study the case.

58 yo female with DM, HTN was admitted on 6/21 for progressive muscle weakness and subsequent fall. She has arrhythmia s/p pacemaker placement, regularly followed up at Taiwan Hospital. She had a left AV shunt placed a month ago to prepare for hemodialysis. She has had oliguria without edema in extremities since 2 months ago. 10 days ago, she developed poor appetite due to post-prandial nausea. In the past 3 days, she developed progressive muscle weakness, culminating to a fall today. She displayed no consciousness change, fever, or abdominal pain.

Her vitals signs were normal. Her physical exam had mostly negative findings. One pertinent negative was “no edema in extremities,” which is a possible presentation late stage renal insufficiency. However, her lab values showed severe hyponatremia (112), hypokalemia (2.5), anemia, elevated creatinine and BUN. The last three could be explained by chronic kidney disease (decreased EPO production and glomerular filtration rate.) The severe hyponatremia and hypokalemia were both concerning and intriguing.

So the clinical impressions were:
1. Hyponatremia
2. Hypokalemia, r/o poor appetite
3. CKD S5, uremic symptoms (uremia could have caused poor appetite, vomiting/nausea)
4. Type II DM
5. HTN (probable complication of CKD)
6. Anemia (probable complication of CKD)
Initial treatment plans were
1. KCl supplement
2. F/O stool OB to check source of blood loss if any
3. Prepare for hemodialysis

The patient also received 3% normal saline at decreasing infusion speed to increase her serum Na+ level gradually. Dr. Chen was careful not to increase serum Na+ too drastically to avoid demyelination syndrome. He reasoned the patient likely had chronic instead of acute hyponatremia. If it were acute, the patient would experience very severe symptoms and would be rushed to ER. Since it most likely was chronic hyponatremia, then the CSF would have equilibrated with the serum osmolarity and Na+ concentration. In other words, the CSF Na+ level was also abnormally low at 112 upon admission. So if the serum Na+ was corrected too quickly, the CSF would not be able to equilibrate immediately (due to BBB.) Then the osmotic difference between the CSF and the serum would cause fluid to rush out of the central nervous system, causing demyelination. This indeed was a very good caution.

While the patient’s serum Na+ increased (going towards normal), her consciousness actually deteriorated. So they consulted the neurologist, who suspected that there might have been demyelination syndrome due to over correction. The brain CT showed no definite lesion and the patient’s consciousness continued to improve. When Dr. Chen and I saw her today (6/28) during rounds, she was fully conscious and conversant, asking to go home. It’s inspiring to witness how Dr. Chen’s knowledge and caution help the patient regain her function. During our visit with the patient, Dr. Chen acknowledged the patient’s desire to be discharged. He also explained to her that he was concerned about her AV shunt might developed a thrombus because her left arm was quite swollen. He also let me feel the thrill on the AV shunt and ascultate the extremely loud bruit!!

Foley training discussion with Dr. Shiu

Dr. Shiu ordered Foley training for this patient and explained to me why the protocol was necessary. Foley catheter is a thin sterile tube inserted through urethra into the bladder to drain urine. After using a Foley catheter for a while, patient cannot be taken off of it without training. This is because the bladder gets used to not being distended and sending the message of urgency to the CNS. So if the patient goes off of F C quickly, he or she may not experience urinary urgency even with extreme bladder distension. For the elderly, sometimes their bladders may expand to hold liters of urine without the patient wanting to urinate. More deceiving is the fact that, pass a certain point of distension, urine will leak out of the urethra from the bladder. So patient may appear to urinate without actually emptying his bladder. This is why it’s important to train the bladder and re-establish the urgency signal to the brain. For this patient, Dr. Shiu instructed clamping the catheter every 2 hours so fluid may build up in the bladder, sending the urgency signal to the brain. Once the patient feels the need to urinate, unclamp the catheter to relieve the pressure.

After rounds, Dr. Chen and I discussed the case in details. In our talk, he’s shown me more than I could ever imagine about the intricacy and complexity of nephrology. We covered the following topics:

• Hypokalemia often manifests in Q wave in EGK, while hyperkalemia shows up as elevated T waves.
• Edema, cardiac gallop sounds, lung basal field crackles are all good indicators of fluid status.
• Hyponatremia types/etiology (mindmap)
• Physiologic (appropriate) vs. non-physiologic (inappropriate) ADH release
• Thyroid hormone, cortisol effects on fluid status
• Electrolyte/fluid status correction and central pontine demyelination (demyelination syndrome)
• Metabolic effects on serum electrolyte
• TTKG (trans-membrane tubular potassium gradient)
• Concentration does not equal amount
o To monitor micro-albuminuria, use U_alb/U_creatinine
o To find amount of K+ excreted, use U_K+/U_creatinine
• Complex renal disease (Glomerular AND tubular dysfunction)
o DM glomerulo-sclerosis =>decreased GFR=>lower K+/Na+ filtration
o Tubular dysfunction=>decreased K+/Na+ reabsorption
• Can’t dilute or concentrate urine well
o Combined G/T disease=> various electrolyte profile (hypo, normal, or hyperkalemia, hyponatremia)
• Medication that cause tubular interstitial damage
o Chinese herb, NSAIDS
• Fanconi syndrome: disease of the proximal renal tubules of the kidney in which glucose, amino acids, uric acid, phosphate and bicarbonate are passed into the urine, instead of being reabsorbed.


Three other patients we visited during rounds.

An 83 yo male presented with change in consciousness. He had no fever or other frank signs. Dr. Chen said 4 ddx we must consider are: sepsis (elderly sometimes don’t mount a strong enough immune response to present fever), medication induced consciousness change, metabolic, and degenerative origin. Patient has suffered dementia and dilution, and he has been on low dose narcotic for his degenerative back pain. Pt’s son brought him to the hospital because he was asleep for long hours and could not wake up for meals. After admission to the hospital, he has been regaining his consciousness, so Dr. Chen discusses with the patient’s son about reducing doses of narcotics and other psychoactive agents.

78 yo patient presented with jaundice due to reaction TB antibiotic treatment and fever. The high bilirubin and low albumin led Dr. Chen to discontinue TB antibiotics temporarily. First urine culture showed Candida; 2nd urine culture showed extended spectrum resistant E. coli. Dr. Chen prescribed Ertapenem, but the patient reacted with seizure. After switching to Myroupenem, the patient has been responding well.

70 yo presented with fever and repeated UTI/leukocytosis. Urine culture showed Klebsiella and ESEL. Dr. Chen prescribed flouroguinolone first and then switched to Ertapenem based on the culture results. Blood culture showed non-resistant E coli, inconsistent with the urine culture. Dr. Chen proposed that perhaps patient had transient bacteremia due to diarrhea (although the Ertapenem would have suppressed the level to less than 10^5.) Dr. Chen emphasized the importance of finding/having an idea of the source of bacteremia. He shared another case to strengthen his point. A DM patient had pyuria and bacteremia but ABD echo had negative findings. Patient continued to spike fever despite of no signs of infection, until CT scan showed a large liver abscess, which explained the bacteremia. Furthermore, U/S detected bilateral hydronephrosis. Dr. Chen said the patient might have a neurogenic, spasmic bladder, so he ordered an intravenous pyelogram to investigate causes of the hydronephrosis. Patient is doing better; fever has subsided with Ertapenem.

8-9am Internal medicine meeting:
ABD pain: incredible differential diagnosis exercise!!!

Dr. Wu was such an incredible teacher. He led us through an exciting journey of differential diagnosis and detective work through a deceivingly simple chief complaint of “abdominal pain.”

Dr. Wu started with the anatomy, which totally confirmed what Dr. Perra recommended us to know well to prepare for all rotation. (I met with Dr. Perra before our trip, and he advised that we needed to know the anatomy well first and foremost.) He said, the origin of epigastric/upper ABD pain could all the structure around this area: pancreas, gall bladder, spleen, stomach (peptic ulcer disease), lung, heart, and even diaphragm. Peptic ulcer disease symptoms often worsen in hunger, so patients usually awake in the middle of the night or early morning in severe pain. PUD patients often have history medication, NSAIDS, steroids use and family history of H. Pylori infection.

He said that inferior wall myocardial infarction could often be referred to epigastric region pain. One must not miss a diagnosis like this. Pleuritis could refer to ABD pain, and the pain would be related to movement and breathing. L diaphragm disease can reflect to epigastric region while R diaphragm may reflect to both shoulders. Gallbladder stone or laceration would be stronger after meals, due to increased peristalsis. GB pain is best described as dull, from anterior to posterior. If gallbladder stone completely obstruct the common bile duct, one should also check the distal biliary bile duct. Blockage of distal biliary bile duct often leads to pancreatitis, which manifests with epigastric pain and elevated serum amylase. Sometimes patients may experience extreme epigastric pain, which subsides with time—this presentation may be explained by an acute obstruction by GB stone, which later passes.
Hepatitis, on the other hand, often does not manifest in referred epigastric pain. This is because there is no nerve in liver parenchyma; nerves run along hepatic vessels. So pain with hepatic origin are usually bloated or swollen in nature; for example, the parenchyma is so inflamed that it starts compressing the peri-vascular nerves. Pain with renal origin may present as ABD pain as well, often due to renal stone. Lastly, one should consider muscle strain and ABD hematoma as ddx for ABD pain.

The resident also noted that the patient had hyperactive bowl sounds. Dr. Wu suggested ileus. The ABD Xray showed slightly more than usual amount of stool. So Dr. Wu brought up a critical point about ABD pain. One should try to gently percuss the ABD to get a sense of the extraneous material: solid (organ enlargement, stool impaction), gas (abscess, pneumobilia), or fluid (ascites). One should pay attention to both the percussion sound and the tactile frequency and vibration.

CT scan can reveal much too. It’s hard to tell in empty stomach if there’s asymmetric wall thickening. But with lumen distention, one can tell if gastric or intestinal lumen has focal thickening, which could indicate neoplasm. With tumor large enough to obstruct GI lumen, distention can be observed proximal to the mass. He also talked about CBD (common bile duct) anatomy further. Adult CBD usually has 7mm diameter, greater than 1cm is considered distention (need to investigate obstruction). One should also compare the sizes of CBD against hepatic portal vein in the same CT slide. If CBD is larger than portal vein, it’s distended with or without exceeding 1cm.

Dr. Wu then elaborated on the branches proximal to CBD, joined from common hepatic duct and cystic (GB) duct. Tracing common hepatic duct back into the liver, there are left and right intra-hepatic ducts. Portal veins run parallel to these branches. Distended biliary tract, including the above branches, can be seen as large hypo-dense area in CT scan. When GB stone is the suspect for CBD distention, one can check serum bilirubin and MRI to confirm.

This was very fun to learn about many of the possible causes of ABD pain and how to analyze backwards from symptoms to etiology.

130-5pm Nephrology outpatient clinic

I made a statistical note this afternoon in Dr. Chen’s clinic. Of the 22 patients he saw today, there were 20 with progressive/chronic renal diseases. 2 cases were UTI’s. The interesting thing was the co-morbidity trend. In the 20 CDK patients, 6 had HTN, 5 had type II diabetes, and 7 had both HTN and t2DM. I want to continue these counts for the rest of the week whenever possible. I also asked Dr. Chen about whether HTN causes CKD. He said that this notion used to be in vogue, but it’s becoming more dubious. Only malignant HTN has been shown to cause nephrosclerosis (pathological proof). The link between essential/isolated HTN with kidney dysfunction is questionable, without pathological proof.

He also said that it would be interesting to look into different specialty’s guidelines for treatment goals. He said that cardiologists pay attention to serum lipid, HTN, serum glucose, etc. Nephrologists heed renal function, and glucose, and HTN, etc. Hepatologists care about HTN, lipid levels in addition to liver functions. So there are overlaps between the specialties but they have slightly different take and priority on each parameter and treatment goal. He said that more and more, cardio-renal should be considered as a unit like cardio-pulmonary has been. For instance in late stage renal disease, one should be cautious with ACE-I usage because it can dilate efferent arterioles and further dampens GFR. ACE-I, in early renal disease, can actually protect against glomerular damage from ultra-filtration. If the patient has reached ESRD, ACE-I can be used at higher amounts if necessary to control HTN because the patient no longer relies on his/her own GFR. This is prime example of how renal health is related to cardiovascular health. As I rotate through the different specialty and present the multi-disciplinary case study, I begin to appreciate how profoundly true the first principle osteopathy (the body is a unit) is.

Learning happens when it's fun!

Today is the first day I wrote down more than an index card of notes. There was so much new terminology and interesting concepts that I wrote down several pages of notes within 2 hours. So I’m made a mindmap of the notes; you can view the converted outline here. I’ve also attached an outline format in this blog.

We had so much fun today. Dr. Liao treated Nicole and me to a big lunch: all-you-can-eat BBQ seafood and hotpot during lunch. He even invited Maggie, a female surgical resident, to accompany us to add to our fun conversation and cultural exchange! We had a lot of fun chatting, before and after our long, delicious lunch, we learned quite a bit (as you can tell from the notes) about traumatic neurology. I realized that successful and brilliant people like Dr. Liao have a great sense of humor and a sense of wonder; they love what they do, and can’t stop talking about the field of study they have chosen; they make analogy between their medical specialty and daily life stuff. I begin to see that having fun is the key to success. Passion turning into drudgery is the greatest tragedy of all. Switch task, take a break, go shopping, or hang out with friends—always be refreshed and excited when I encounter new knowledge or skills in medicine and in life. The learning will naturally take place when my mind is fresh and inquisitive.

Trauma Neurology
• + - Glasgow coma scale
o classify head injuries
o evaluate and score the best side
o E
• (best) eye opening
• 1-4 pts
o M
• (best) motor
• 1-6 pts
o V
• best verbal response
• 1-5 pts
o total
• minimum: 3 pts
• max: 15 pts
o head injury classification
• minimal
• 15
• clear consciousness w/o prolonged neuro deficit
• no LOC, on amnesia
• discharge w/ head injury sheet
• frank vomiting
• sign of increase ICP
• pupil enlarge
• seizures
• no pain meds stronger than tylenol
• no asprin
• CSF leak
• rhinorhea, otorhhea
• minor
• skull x ray
• not senitive to hemorrhage
• (-) observe for 6 hrs
• (+) head CT
• pt history
• age>65, anticoagulant
• present illness
• mild
• 14
• moderate
• 9-13
• often deteriorate
• severe
• severe
• 6-8
• 3-5
• + - Monro- Kellie doctrine
o brain
o CSF
o blood
• hyperemia
• CO2 retention triggers cerebral vaso-dilation
• more blood in the brain
• ICP
• obstruct venous outflow
• CO2 retention
• more dilation
• CBF
• cerebral blood flow
• k(MAP-ICP) d^4/ (8* length* viscocity)
• modified F = ΔP π r 4 / 8 η l
• laminar blood flow
• clinically we manage MAP, ICP to control CBF (CPP)
• 3 H's
• hypertensive tx
• hypervolumia
• hemodilution
• not necessary in most trauma pts due to blood loss (blood is already thin)
• dilation cascade
• vicious cycle
• brain herniate
• trans-tentorial hernia
• or out of foramen magnum
• dilate
• constrict vaso
• mannitol/hypertonic saline
• draw cerebral ECF into circulation, remove from brain
• IICP
• surgical decompression
• maitain physiologic parameters at normal ranges
• lesion, hematoma removal
• ventriostomy
• sedation
• lower intrathoracic, ABD pressure
• CCP
• increase CCP w/ colloid infusion
• vasopressin=hypertensive tx
• cerebral blood V
• elevate head
• head neutral
• head turning collapse IJV, prevents venous retunr
• repeate 1-4
o others
• brain edema
• trauma, cytotoxic, vasogenic
• hydrocephalus
• less due to trauma
• more due to vascular problem
o hyperemia vs. brain edema
• hyperemia
• cerebral perfusion
• SjO2 <50% • hypoperfusion • SjO2 >80%
• hyperperfusion
• =hyperemia
• jugular venous O2 sat
• =too much blood passes thru brain w/o brain extracting O2
• jugular [lactate]
• =decrease anearobic respiration
• brain edema
• hypo-perfusion to brain
• [lactate] due to less O2 supply to brain
• both have IICP
• ICP monitor can help distinguish the 2
• + - brain resusitiation
o "squeeze (oxygenated) blood into swollen brain)
o patient suffers increase intracranial pressure
• cerebral blood flow
• cerebral perfusion pressure
• manage by increasing MAP
o CPP cerebral perfusion pressure
• =MAP (mean arterial pressure)- ICP (intracranial pressure)
• so if ICP higher
• tranditionally increases MAP aggressively to maintina ICP
• but aggressive vasopressor to increase MAP risk CV collapse
• + - brain injury
o + - by mechanism
• contact (blow)
• focal lesion
• eg. fracture, contusions, lacerations, hemorrhage
• acceleration/deceleration
• eg. whiplash
• diffuse (axonal) injury
• spectrum mild to severe
• physiological -->pathologic disturbances
• small petechia--> prolonged LOC (loss of consciousness)
• axis of rotation (center of gravity)
• more severe shear injury
o + - by stage
• primary
• causes by the above mechanisms
• hematomas
• epidural
• best progonsis, b/c dura's intact, protects brain
• sources
• middle menigial artery
• sigmoid sinus
• venous EDH
• subdural
• sources
• briding veins b/w dura and brain
• brain contusion, brain superficial blood vessels
• couter coup intracranial hemorrhage
• tx
• craniectomy
• store skull bone subcutaneously
• dura-plasty
• w/ external periosteum
• expand dura capacity to buffer ICP increase while brain heals
• ICP monitor
• restore live-preserved skull fragment to the cranium
• skull closure
• CCI
• =counter coup injury
• analogy
• 80% full bottle
• when hit from the bottom, the water near the air/fluid interface moves the most
• more mov't, greater injury
• occiput grounded fall
• frontal CCI
• frontal base, temporal tip
• frontal skull more tortuous than occiput
• frontal grounded fall
• less occipital CCI
• b/c occiput is smoother
• parenchymal
• intraventricular
• hypertensive intracranial hemorrhage
• hematoma signs
• racoon's eyes
• anterior cranial fossa
• battle sign
• middle cranial fossa near petrous ridge of temporal bone
• secondary
• tissue reaction to primary injury
• systemic condition caused by primary injury
• eg. ischemia, stroke
• brain's reponse to injury is more dramatic than rest of body
• inflammation, hyperemia
• + - CCP demand
o sedation
• less work for brain/body voluntary movement
o paralysis
• conscious m't controlled by brain
o hypothermia tx
• metabolic rate
• lower than body temperature, more infection
• hence controversial
o sugar control
• avoid hyperglyacemia
• avoid hypoglycemia
o prevent seizure
• seizures require lots of ATP, increase metabolic rate
• + - CCP supply
o old time
• aggressively increase MAP to counter IICP
• risk, lung edema, cerebral hemorrhaging
• large V fluid in fluid out
• up to 1L/hr
• electrolyte imbalance
• frequent blood test
o now
• CPP maintain at 60 mmHg
• less aggressive
• tx underlying IICP cause
• remove lesion/hematoma ASAP
• normalize physio parameters
• need good baseline cardio-pulmonary-renal fxn to save brain
o manage
• if ICP>20 mmHg
• CSF drainage
• sedation (decrease CCP demand)
• mannitol (decrease ICP)
• hyperventilation
• lower CO2 pressure
• encourage cerebral vasoconstriction
• don't go too far or compromise CBF
• brain CT, pre-op
• delayed hemorrhage
• stroke after injury (esp. atherosclerotic pt)
o ICP
• head up 30 degree
• neutral, non-rotated head
• PaCO2 35-40
• PaO2 100
• sedation especially for pain, derease energy demand
• gentle nursing care
• sedation prior to uncomfortable, painful care
• Na 140-145
• burnt patient may have hyponatremia
• not too high, >155 may cause arrythmia
• seizure control
• dilantin
• mannitol/hypertonic saline
• draw cerebral ECF fluid into circulation
• + - prognosis depends on
o age "remaining viable/ functional brain"
o parenchymal damage, more severe than epidural damage
o 2nd insults
• hypoxia, shock, metabolic
• metabolic encephalopathy
• hyperglycemia
• alter biochemistry in brain cells
• cell death
• hypoglycemia
• energy deficit
o ABC
• airway, breathing, circulation
• + - mneumonics
o external carotid branches
• "Some Attendings Like Freaking Out Potential Medical Students."
superior thyroid, ascending pharyngeal, lingual, facial, occipital, posterior auricular, maxillary, superficial temporal
o coma ddx
• AEIOU TIPS
Alcohol, encephalopathy, insulin, opioids/other drugs, uremia, trauma, infection/inflammation, psychiatric, syncope
o ER/Trauma Hx
• AMPLE
• allergy, medicatio, past medical Hx/pregnancy, last meal, event (precipitating)
• + - cases
o infected craniotomy
• 10 cranial surgery to treat infection
• pt still expired
o hyperglycemia pt
o intoxication
• cocaine
• seizure related to drugs
• alchohol withdrawal
• sympathethomimetics
• cocaine, methamphetamine
• intravascular vasculitis, untractable seizures
• doesn't exclude additional causes
• drunk patient may also have head trauma
•
• sedative+alchohol
• may cause airway obstruction
o TCD
• no net cerebral flow
• anisocoria
• uneqaul pupil size
• ET intubation, hyperventilation, mannitol
• cerebral net flow
• CS score
• craniectomy
o open skull fracture
• pneumocephalus
• dx procedure
• massive CSF leak
• air enter into brain
o aged M
• frequent falling
• brain tumor obstruct ventricle outlet
• distended ventricles
o serial brain CTs
• 6 hrs
• EDH, SDH, ICH
• dangerously high ICP
• remove infarcted brain
o delayed ICH
• R hemi-dysplagia
• + - hospital care
o ABCD
• airway
• breathing
• circulation
• disability
o baseline ABCD
• CHF, COPD, old CVA
o CPR vs CPCR
• intubate if GSD<8 • confirm CS injury • adminster sedatation before intubation o more urgent to head truma • Cardio thoraci trauma with ABC problems • airway compromise o quick id of assocaited trauma • massive nasal oral bleeding • pelvic bleeding • external fixation, tran-catherter arterial embolization • thighs: packing, suture • ABD trauma • simultaneous operation • + - radiological exam o plain films • portabl unit • open mouth (atlanta-axio joint) • "odontoid view" • CXR • pelvis Xray for total hip relpacement o CT • must have stable vital sign • at least 10 minute • shoudl scan all suspicious parts simultaneously • ABD, lower chest, pelvis • facial/C spine o no need • alert, awake, normal neurology, no distracting injuryng • no neck pain, mental status changes • + - trauma guidelines o ABCDE • E: enviromental exposure o high risk • EMT applies collar (C spine protection) o prolonged immobilization • if normal=> may remove collar
• not all injuries need fixation
o wear collar
• if pt's neck muscle is spasmic
• can't visualize the whole C spine
o monoplegia
• brachial plexus injury
• + - 1st tier tx
o gentle care
• w/o sedation
• ICP
• CPP
• >5 minutes of IICP
• nursing activity
• retaping of intubation
o fever
• metabolic rate, inflammation
• more water production
• ICP
o irritable patient
o improper position, sedation
• taper sedation gradually
• keep sedation until day of extubation
• NMB
• neuro-muscular block
• short acting
o rebound IICP
• intermittent mannitol
• now mannitol PRN
o propofol infusion
• anesthetic
• dipropyl phenol
• lipid soluable
• dissolved in water by soymilke
• propofol infusion syndrome
• younger pt insufficient lipid metabolism
• intermittent dose
• rebound ICP
• now continuous infusion
o hyperventilation
• hyopcapnia
• cerebral vaso-constrict
• but avoid hypercapnia
• cerebral vaso-dilate
• ICP
o intraventricular catheter
• IVC
• CSF drain
• bacterial infection higher than fibrostic monitor
o not synchronize w/ ventilation
• pt inspire when machine not delivering O2
• + - 2nd tier
o hypertensive
• blood pressure balance
• bleeding vs. perfusion
o hypothermia
o craniectomy
• don't put the skull bone back during 1st surgery
• +ICP monitor
• 1-3 days
• decompress one side
• after 1 surgery
• IICP persists
• 2nd cranietomoy
• ICP doesn't tell the whole story
• w/o ICP, neurological diseases worsen
• decompressive craniectomy
• frontal, temporal, parietal, lateral flap
• bi-frontal
• smaller window than lateral lesion side
• ICP return to normal
o hyperventialtion
o barbiturate coma
• or increase, more typeso f sedateive
o hypertonic saline
• + - summary
o 15: no medical tx
o 20: meds, NMB
o 30: aggressive tx
o 40: another CT, operation
• decompressive measures
• remove bone
• open dura (duraplasty)
• volume of skull removed accomodate IICP
• close skin
• insert ICP monitor
• pre-op
• poor diastolic perfusion
• post-op
• good dialstoic perfusion
o persistent >40
• bad prognosis
• frank lobectomy
• frontal lobe syndrome
• brain contusion
• mostly superficial

Decompression for the brain and for the mind.

Dr. Liao (chief of neurosurgery) first took me to remove a tracheo-tube from a patient who had two brain surgeries due to a traffic accident. This 59-year-old female was admitted to the ER with a subdural hematoma and severe scalp lacerations. The hematoma was nearly .8cm in the CT scan near her left frontal-temporal region. The midline of the brain was shifted nearly 1cm over to the right, (larger than the size of the hematoma), indicating a brain tissue reaction, most likely hyperemia to the trauma. So Dr. Liao performed a decompressive craniotomy to remove the hematoma. He also removed a segment of cranial bone and embedded it in the patient’s left lower abdominal subcutaneously. After the cranial bone removal, he performed a dura-plasty to expand the intracranial space to allow the brain to heal without secondary injury from increasing intracranial pressure. He used an autograph in the dura-plasty by extracting the outer-periosteum from the patient’s exposed scalp. He could have sent the segment of skull he cut out to be frozen for preservation until the patient’s healed and ready to put the skull bone back. However, he chose to preserve her skull bone subcutaneously in her left abdominal region so that the bone would be alive. He explained that the freezing process would form crystalline water, which would pierce through osteocytes and kill the living bone tissues. If the bone segment was frozen rather than subcutaneously embedded, it would be innominate upon the cranium reconstruction surgery. The dead piece of skull would be just a bridge for the living cranial bones around it; it would depend on the osteophytes to grow into it. I admire how Dr. Liao opted for a longer surgery because it would preserve the patient’s bone better than the freezing option.

A couple interesting terms I noticed while scanning the patient’s chart
1. Bovie stops bleeder during craniotomy. Bovie is the inventor and commonly used informal name for electrosurgery. Electrosuergy applies a high-frequency electric current to biological tissue as a means to cut, coagulate, desiccate, or fulgurate tissue.
2. Galea suture is made by “few pairs of oblique holes (made by drilling in the surface cortex of the bone flap) through which suture materials may pass. The galea aponeurotica is sutured to the bone flap by means of these holes. These galea-cranium sutures reduce the subgaleal free space in which pooling of CSF or hematoma may occur.” (pubmed article) http://www.ncbi.nlm.nih.gov/pubmed/10481444
3. Silastic sheet: I researched about this and found it in preventing keloid scar formation in plastic surgery. From the context of the patient’s chart, it sounded like the silastic sheet was placed between the patient’s scalp layers during the first surgery. It helped the surgeon separate the layers more easily during the second surgery. I will ask Dr. Liao about why and how he used the silastic sheet on this patient.
4. Hemostasis by monopolar coagulator before wound closure.

He also took me to the ICU, updating me on the patient who’s had continuous ICP monitoring with an intraparenchymal fibroptic probe inserted through a cranial bolt. He said in general we were more concerned about the lower threshold for cerebral perfusion pressure than the higher limit. A low CPP can lead to brain ischemia and subsequent infarction. From the monitor, one can see that CCP is the difference between arterial pressure and the ICP (intra-cranial pressure). He also pointed out to me the difference between an arterial versus a venous catheter. The arterial tubing was a lot more rigid and smaller caliber than the venous one, which were engineered to mimic human vessels. Also he said that surgeons liked to insert catheters away from the surgical sites. This meant craniotomy often has femoral vein catherization to prevent collapse of medication tube during surgery; lumbar spinal procedures have subclavian catheter. He also showed me CT scan of the pelvic vessels—NAVEY (femoral nerve, artery, vein, empty space, and lymphatic’s). The CT scan was captured during arterial phase, so we could see the round femoral artery light up, while the larger caliber, collapsed vein rest against it. It’s generally more challenging to catherterize femoral vein than the subclavian vein due to its smaller caliber, but the latter risks pneumothorax.

Venous infarction
Another interesting concept he mentioned today was venous infarction, quite unique to the brain. Infarction following ischemia in most of the body often is due to lack of blood supply from arterial blockage. However in the brain, you can have infarction caused by venous stasis. This is because the brain has very few lymphatic vessels, and it depends solely on the venous system to drain its blood supply. So if there is a venous blockage, for example due to venous thrombosis, venous pressure would build up relentlessly. Due to the rigidity of the skull and incompressibility of cranial composition, the arterioles would be compressed as venous pressures hikes up. This leads to decreased supply of oxygenated arterial blood entering the brain, hence ischemia and infarction.

Lunch meeting:
Documentary on Herceptin (targets HER2 receptors on breast cancer cells) The movie was very touching and uplifting. I did not finish watching due to the surgery but would love to watch it later.

L3/L4 decompression surgery
Dr. Ding had me scrub in to assist him with the procedure. It was a great honor and pleasure. The case turned out to be more complicated than expected because the disc was completely degenerated and the nerve root got squeezed out laterally. This meant that the patient had lived with the herniated disc symptoms for a while, more than a couple months. It was 2 inches deep before we reached the transverse processes. Dr. Ding removed the deformed disc in bits and pieces. He then soaked the wound with morphine and steroids. I look forward to visiting the patient tomorrow to follow up on post surgical recovery.

Neuro mnemonics of the day
“SCALP” (5 layers of the tissue surrounding the brain): Skin, connective tissue, aponeurosis (epicranial aponeurosis), loose connective tissue, periosteum.

State of Mind

State of Mind

Surgical department meeting-CRC chemotherapy presentation by TTY Biopharm company.

It was great to review and get new updates on colorectal cancer chemotherapy. Several interesting points included,
1. FOLFIRI (Ironotecan+5FU+LV) needs lower dosage of Irinotecan (single agent), this helps minimize the toxicity. Irinotecan when used alone at high dosage causes 12% sepsis.
2. Uracil competes with 5FU metabolism. So Uracil can increase 5FU half-life.
3. UFUR (Uracil-Tegafur) has numerous advantages over 5FU: oral, less toxicity than infusin 5FU (less hand-foot syndrome), good for low dose long term usage to suppress tumor angiogenesis, reduce recurrence and prolong lifespan.

Neuro-surgery
First time assisting in surgery
C4/C5 disc herniation, disc removal, spinal nerve decompression and prosthetic disc insertion. Dr. Ding, the neurosurgeon of the case was very encouraging and patient. He taught Nicole and me step by step how to achieve the highest standards in aseptic practice (our patient was receiving a prosthetic disc implant today so aseptic practice was absolutely critical). The steps were
1. Scrub with iodinated soup up to the elbows, make sure to leather up a lot of bubbles
2. Rinse off the first scrub
3. Apply a second scrub, leave the soapy bubbles on
4. Make sure to hold hands up with elbows close to your body, leaving the most distal part of your upper limb higher than the more proximal part (this will ensure “dirty” water dribbles down and way from your hands, keeping your hands the cleanest
5. Dry your self with 2 aseptic towels, starting from the most distal (digits) than work your way up your arms without touching your hands to your arms (you can fold the towel diagonally and then warp it around your wrist, while pinching the two farthest points of the towel with your other hand)
6. Put on aseptic scrub, nurses will assist with tying it in the back for you.
7. Put on aseptic gloves with scrub sleeves inside the gloves to make sure no bare skin is exposed.
8. The area between your clavicles and the stomach is considered aseptic zone; never leave your hands outside of this zone.
He let Nicole and I took the first assistant’s position (this is a spot that only 4th year resident and above have the privilege of standing in during surgery). We took turn in assisting-- holding various tools in place, suctioning the blood and fluid away, and syringe-dripping saline to cool off the tissues while the high-speed electric drill was going through the vertebrae. We looked under the microscope during the surgery as well. The nurses were very nice to us too. I notice what a great relationship doctors and nurses have in Taiwan. They respect and appreciate one other genuinely. Dr. Ding also said that it was the nurses who taught him how to perform aseptic scrubbing in great details.

Brain CT discussion Tentorial subdural hemorrhage
On the CT scan, we could see that hemorrhage was less dense then skull but denser than brain tissues. So it showed up lighter than the brain and darker than the skull.

Diagnosis:
Timing/ sequence is crucial.
Cerebral vascular rupture=> stroke=> MVA
Or MVA=>subarachnoid hemorrhage
Pt Hx: no vascular disease (no HTN, no DM), unlikely spontaneous cerebral vascular rupture, MVA trauma induced subarachnoid hemorrhage more likely

Complications
1. Seizures
a. Acute seizure, within 24 hours-3 days
b. Delayed, after 3 days
c. If no acute seizure, likelihood for delayed seizure is lower
2. Delayed hemorrhage: after 3 days
3. Hydrocephaly
a. Obstruction of CSF resorption through the cerebral sinus
b. Anytime: hours, days, months, years
c. Gradual, not emergent
d. Signs: incontinence, dementia, and unsteady gait
4. Chronic subarachnoid hemorrhage
a. Elderly patient: brain atrophies
b. Hemorrhage is normally resorbed w/ micro-vessels
c. Atrophied brain has les
5. Vaso-spastic stroke/ischemia

Several other topics he covered were (details supplemented with wikipedia content)
1. Sylvan fissure/ lateral sulcus divides the frontal lobe and parietal lobe above from the temporal lobe below. It is in both hemispheres of the brain but is longer in the left hemisphere.
2. The Circle of Willis comprises the following arteries
Anterior cerebral artery (left and right)
Anterior communicating artery
Internal carotid artery (left and right)
Posterior cerebral artery (left and right)
Posterior communicating artery (left and right)
3. 2 in 3 out (sensory in through optic nerve, motor-extraocular movement via oculomotor nerve)
4. 4 in 5 out (Corneal reflex is conducted along with the facial nerve section of the test. Note the sensory innervations of the cornea is provided by the trigeminal nerve while the motor innervation for blinking the eye is provided by the facial nerve)
5. Caloric test: Cold or warm water or air is irrigated into the external auditory canal, usually using a syringe. The temperature difference between the body and the injected water creates a convective current in the endolymph of the nearby horizontal semicircular canal. Hot and cold water produce currents in opposite directions and therefore a horizontal nystagmus in opposite directions.[4] In patients with an intact brainstem:
• If the water is warm (44°C or above) endolymph in the ipsilateral horizontal canal rises, causing an increased rate of firing in the vestibular afferent nerve. This situation mimics a head turn to the ipsilateral side. Both eyes will turn toward the contralateral ear, with horizontal nystagmus to the ipsilateral ear.
• If the water is cold, relative to body temperature (30°C or below (ice water)), the endolymph falls within the semicircular canal, decreasing the rate of vestibular afferent firing. The eyes then turn toward the ipsilateral ear, with horizontal nystagmus (quick horizontal eye movements) to the contralateral ear.[5][6]
• Absent reactive eye movement suggests vestibular weakness of the horizontal semicircular canal of the side being stimulated.
6. The vestibulo-ocular reflex (VOR) or oculovestibular reflex is a reflex eye movement that stabilizes images on the retina during head movement by producing an eye movement in the direction opposite to head movement, thus preserving the image on the center of the visual field. Doll’s eye sign, eyes moving away from the direction of head movement shows that a comatose patient’s brain stem is intact.

L3/L4 disc herniation, decompression surgery consultation with patient’s wife
Dr. Ding patiently went over the MRI scan of the herniated disc in L3/L4. He assured the patient’s wife that they would operate tomorrow. He recommended bilateral disc decompression because patient had symptoms in both legs—numbness, pain, and weakness.

Evening outpatient Clinic with Dr. Chen
Patient with central epigastric pain, relieved by leaning forward. Classical signs of pancreatitis. Elevated amylase and lipase in last report (May) but she was too busy to make F/U appointment with the GI doctor. GB stones may have obstructed the common bile duct, causing enzymatic juice back up into the pancreas, hence pancreatitis. This patient may have developed chronic pancreatitis, so she needed to go to the emergency room to recheck her current enzyme levels.

Dr. Ding is the 5th doctor who told us that medicine is a marathon. We will spend our whole life learning and practicing it. He told us to take it easy, get a feel of what neurosurgery is about and enjoy the learning. He said that when he was a 4th year medical student, he studied an enormous surgical text from first to last page and spent time memorizing surgeon’s configuration of their surgical tools and setup. He realized in hindsight that he needn’t do these things because all learning and challenges will come in due time. I am grateful for these words of wisdom—to prepare my mind for life-long learning. I need not rush to expand my knowledge; a curious and well-rested mind is the most efficient sponge of all!

Work and play

This morning I met with Dr. Chen (oncologist) to go over our group presentation on CRC. He was incredibly helpful. He not only helped me improve my section on the oncologist’s approach to the case, he also modified the rest of the presentation. He also helped us obtain numerous laboratory studies, including CBC, serum CEA, chemistry panels and imaging studies: paneoscopy, colonoscopy, chest Xray, CT scan, ABD U/S, and colonoscopic biopsy. He contacted various departments to gather as all the pertinent data. I could not believe how generous he was with his advice and assistance. I was excited to learn a logical and comprehensive structure of a case presentation. The general flow for a cancer case presentation should be:
1. Chief complaint (include pertinent history of present illness)
2. Physical exam
3. Clinical impressions
4. Differential diagnosis
5. Lab studies
6. Imaging studies
7. Rule in and rule out DDX based on findings
8. Treatment (surgery, chemotherapy, radiation) and rationale
9. Follow up and treatment-induced changes
10. Survivorship

After lunch, my new preceptor Dr. Liao, a neurosurgeon brought Nicole and me to the ICU. He showed us how to read a CSF monitoring machine. There was a wave representing the mean intracranial pressure, another wave represented the arterial pressure. On this patient, Dr. Liao performed an emergency craniotomy to remove an intra-cranial hematoma 1am-5am this morning.

He then presented different intra-cranial shunts, including epidural, sub-arachnoid, intra-dural, and brain parenchymal devices. He taught us that the cranium includes 4 types of material: brain, fluid, blood, and something else. When one of the four component increases in volume, the other three components decrease or get compressed. For instance, if there is a tumor or bacterial abscess (something else), volume of blood and CSF will decrease while the brain tissue gets compressed. He also showed us that slight changes in CSF volume increases intracranial pressure slightly. However, once above a small volume threshold, intracranial pressure increases exponentially with small increase in fluid volume. This is because the skull is rigid and allows for negligible expansion.
We worked hard over the weekend on the case presentation, so we decided to go out tonight. It was lots of fun, Taipei 101, Ding Tai Fong, and night market. We’ll all sleep very well tonight after all the good food, sight seeing and strolling pass stands and little shops all night!

In My Heart of Hearts.

I was going to write about an abdominal aortic aneurysm case through the patient’s point of view. After one paragraph, I realized that I was still writing about a case, only in first rather than third person. As much as I read over his file and learned about his medical history, I had learned merely about one aspect of his life in great details, while knowing very little about the person that he is. My attempt to write from the patient’s perspective helps me become more aware of the physician-patient relationship. A doctor often has the most pertinent information regarding her patient’s health, merely an initial/ admitting interview includes family history, social history, sexual history, and much information that no one shares with a stranger in brief encounters other than a medical interview. The doctor tries to learn about everything about the patient that assists their medical diagnosis and treatment. To have the patient’s best interest at heart at all time is not easiest thing. For instance, where do you draw the line between whether an interview question is out of intellectual curiosity or out of medical necessity? How do you decide if a medical procedure needs to be done when the mortality rate of the procedure is 70% and that without the said procedure is 100%? I don’t exactly have the answer for my musing. From what I observed in Taipei hospital, I see that all healthcare providers here put their patients best interest at heart and they genuinely respect their patients’ wishes.

The procedure to repair the AAA was an incredibly intricate and challenging procedure. It was a great honor to witness it. The 78-year-old male patient had ESRD and CAD. His AAA was largest at 6.5 cm diameter. Dr. Chen, the CV surgeon, invited his mentor/professor to observe and advise at the OR. Both femoral arteries were opened; stent was inserted in 3 separate segments. Balloons were inflated to press the stents against the blood vessels. Finally artificial grafts were inserted within the fixed stents. The operation took nearly four hours. I asked about the long-term effectiveness of these operations, Dr. Fong (cardiologist) stated that these procedures are so young that, there has not been follow up studies about the durability and benefits 10-20 years post operation.

The observation room was packed with cardiologists, nurses, and residents. This was the second such case this year in Taipei Hospital. Sandy, Nicole, and I felt very fortunate to be watching real time radiography of the procedure. After the stent and graph were both in place, Dr. Chen even asked us to enter the OR so he could show us the femoral arteries before he closed up the incision.

This week had been lots of fun and reflection; I saw much that I’d only dreamed about and seen on TV. My respect and admiration for cardiologist and cardiovascular surgeons have grown much with what I have witnessed first hand. In the years to come, I hope to nourish and pass on the passion, dedication, and fearlessness they have instilled in me during this brief yet impactful rotation.

Brave heart, tender heart.

Dr. Chen started our day with a presentation on the ECMO (extra-corporeal membranous oxgenation). He showed us the basic set up, veno-arterial (VA) and veno-venous (VV). For the venous arteriole set up, a catheter connected to a pump (artificial heart) draws blood from the femoral vein). The blood goes through the a heater (to maintain body temperature) and the oxgenator (artificial lung); then the fully oxgenated blood returns to the patient via femoral artery. The VA system provides both supportive heart and lung functions, while the VV ECMO provides ventilation without the damage to the lungs caused by mechanical ventilation. Taiwan government supports and pays for ECMO treatment. Dr. Chen says that ECMO is a very good supportive treatment which buys patients time to heal or to receive transplant. He says that infants and children usually benefit more from ECMO because they often heal better and regain their own cardiac and pulmonary function. In adults, ECMO are often used in ARDS and or heart failure, which often deteriorate and can't reverse its course.

The only female cardiovascular surgical resident Dr. Yu gave a presentation on a review article of ECMO. She presented the costs and benefits of ECMO. ECOM is expensive and requires highly trained personnel to implement. It also requires anti-coagulation because the circuit, especially the membranous gas exchange compartment is highly thrombogenic. Dr. Yu also talked about pumpless extracorporeal interventional lung assist in patients with acute respiratory distress syndrome. It is passive flow system without the artificial cardiac function of AV ECMO. It is good for CO2 removal but not oxygenation, so for respiratory compromised patient, intubated-ventilation needs to be used in conjunction with ECMO.

After Dr. Yu’s presentation, Dr. Chen added that if a patient with severe cerebral injury requires ECMO, he may have to administer ECMO without heparin to avoid cerebral hemorrhage. But a patient usually can not rely on ECMO for heart function over two weeks. VAD (ventricular assistance device) can buy a heart-failure patient more time when waiting for a cardiac transplant.

Dr. Yu took us on rounds. The cases were PDA (peripheral arterial disease), AAA (abdominal aortic aneurysm), DVT (deep vein thrombosis), and OHS (occluded hemodialysis shunt). The PDA patient also suffers from severe microcytic anemia possibly due to iron deficiency. Dr. Yu was originally planning to perform angiography and balloon angioplasty on this patient tomorrow. But in their discussion, the patient expressed that he wanted to address his anemia first before getting lower limb angiography. Dr. Yu supported the patient’s wish without a hint of pressure. His genuine respect for his patients and his exquisite command of medicine exemplify the ideal physician. The AAA patient was an elderly man, with a kind and peaceful smile; he let us feel the pulsation on his upper right ABD. Dr. Yu said that the AAA diameter was 6.5 cm. He will insert a stent to fortify the vascular wall tomorrow. He said that the operation room does not have the equipment for general anesthesia, so he is slightly concerned about patient’s movement or awaking during the procedure. Instead of general anesthesia, Dr. Chen will apply local anesthesia and IV to help the patient sleep during the procedure. In a similar but more complicated case, which required a double stent (aorta and iliac artery), the patient moved his extremities around in sleep on the operation table. Although this past experience made Dr. Chen slightly nervous, he says tomorrow’s aortic stent should be fine. I admire the fact that he works with the equipment available and demonstrates incredible skills and elegance in his work. The ability to deliver the best medical care in all situations should be all healthcare providers’ goal. I am glad to witness how it is done, by so many dedicated and improvising physicians at Taipei Hospital.

The DVT onset was acute, so Dr. Chen administered thrombolytic drugs first. On average, the downstream swelling caused by the thrombotic occlusion resolve with 3-5 days of thrombolytic treatment. The patient’s progress was not satisfactory, so Dr. Chen increased the dosage today. He also discussed the possibility of thrombectomy with the patient. There were several cases of OHS. There are 3 main types of hemodialysis vascular access (hemodialysis shunt): AV fistula, AV graft, and venous catheter. Dr. Chen performed clot removal from both AV fistula and AV graft. In both cases, he used local anesthesia and small incision, suctioned the thrombus out, checked the vascular lumen with angiography, and performed angioplasty when necessary. One case had a more severe occlusion, one of the clot removed was a “white thrombus,” with organization and re-canalization. There was a lumen within the organized thrombus! This brought me back to Dr. Liisa Russell’s pathology lectures, when she emphasized several times the difference between fresh and old thrombus. He also replaced a venous catheter, executing roughly the same steps. He then treated Sandy, Nicole, I, and the cath lab staff to delicious lunch boxes.

In the afternoon, Sandy and I shadowed Dr. Chen (Cardiology Chief) in his outpatient clinic. In addition to reviewing some HTN, CAD, DM drugs, learned 2 main principles. One, the Taiwan national health care insurance and electronic medical files make healthcare incredibly efficient and assessable for the public. Patients see Dr. Chen, can get blood tests, echocardiogram, chest Xray, EKG results back the same day. After seeing the patient, Dr. Chen will help them order diagnostic tests, the patient will return to Dr. Chen’s office to discuss the results in as short as 1 hour. Many patients had been seeing Dr. Chen for awhile, managing long term CV diseases. But even new patients could get focused cardiac exam, preliminary diagnostic tests (EKG, chest Xray), and test result follow up in ONE afternoon. Dr. Chen saw nearly 80 patients this afternoon without compromising the quality of care the slightest bit.

Second, many Taiwanese doctors believe in caring for their patients as whole and unique persons. Cardiologists or oncologists, they all commit to their patient’s complete well being, body, mind, and soul. Both Dr. Chen’s (chief cardiologist and chief oncologist) expressed that an essential part of their job, aside from delivery accurate diagnosis and optimal treatment, was “psychotherapy.” Dr. Chen said, many patients who were referred to him with “chest pain,” did not have true CAD disease. The 2 most common non-cardiac etiologies include autonomic nerve disturbance (due to stress or congenital nerve abnormality) and neurosis (psychological need for support, medical or otherwise.) I saw one patient like this today; his daughter accompanied him to the clinic. She said that he had been seeing many doctors, who looked into almost all his major systems and found no problems. She said that another doctor referred them to Dr. Chen because he was known for his patience with elderly patients. Cardiac exam, EKG, and chest radiograph led Dr. Chen to reassure the elderly man that he was quite healthy. Then, the daughter, Dr. Chen, the nurse, and the volunteer, all reassured him again. I noticed the elderly man’s feet were dark purple with patches of redness and asked Dr. Chen. He explained to me that he was a fisherman and suffered chronic inflammation due to exposure to harsh conditions of UV light, wind, salt water, and pollutants so his feet were hyper-pigmented. He reminded the patient to wear socks to protect his feet before the daughter, with great relief, wheeled her father out.

The cardiology chief, CV surgeon, attending cardiologist and the resident are all brave hearts—they dauntlessly complete 12-15 years of medical training and fearlessly embrace intellectual challenges and operational complexities. They are also tender hearts—they care for patients beyond the organ system that they study and persist to finish nearly impossible procedures regardless of fixed compensation. I marvel daily at this amazing opportunity to be amongst such individuals.

Not for the Faint of Heart

Ella called this morning; she asked me if everything was fine. I replied, "Everything is fine; Mommy is learning a lot." She sang many songs for me. One particular song rang in my ear throughout the day, "Love is something you give it away, you give it away... It all comes back more." I have not had much continuous sleep since I arrived, probably because I'm too excited about all the adventures and learning opportunities ach day presents. I often wake up around 5am; I listen to Goljan's pathology audio is with my eyes closed, falling in and out of sleep and catching little bits of treasured pathophysiology. I was feeling quite tired last night after a nearly 12 hour day. Ella's singing this morning was the best energy booster.

At the internal medicine meeting, a patient admitted due to fever and lower back/lower ABD pain had been sporadically self treating with steroids containing supplement. She was diagnosed with Batter's Syndrome and Steroid-induced Cushing's Syndrome. Upon physical exam, she claimed lower right ABD pain when deep pressure was applied. However, the CT did not show appendicitis. So the resident focused on treating her fever, with antibiotics. The attending recommended administering dexamethasone, because the fever may be related to steroid use withdrawal.

At the meeting, Dr. Tu asks me if I want to observe a pacemaker insertion for a 91 year old patient. My heart nearly jumps out of my throat with excitement. I am very grateful that he is willing to let Sandy and I follow him closely in the OR. We all wear full armor of lead suit, in 3 pieces, apron, vest, and the thyroid cover. Then we scrub in with iodinated soap (it’s our first time!) Dr. Tu explains that pacemaker, once inserted, stay in the patient for 10 years until batteries run out. So it is crucial to practice stringent aseptic techniques. He methodically and gingerly prepares the patient, putting numerous layers of sterile clothes around the pre-marked incision site. He injects 1 to 1 normal saline/Lidocaine subcutaneously along the incision line. Pulling back the syringe each time to check that he does not puncture a vessel, he injects small subcutaneous pocket of lidocaine. He makes a clean cut and then uses blunt dissection to separate the tissue, "this will avoid injuring important structures." I realize the dissection techniques Dr. Eliot and Mr. Silverman emphasized in anatomy are very useful in surgery.

This case turns out to be very challenging. It takes 3 hours more than the original estimated time. The patient's old age has made her heart and vessels difficult to navigate. The vessels lengthen and become more tortuous with age. Because her 3rd degree complete AV block indicates for dual electrodes, one in the left ventricle, one in the left atrium, the case is even more complex. Dr. Tu starts with 1 puncture for two guide wires/leads. But the space within the vessels and heart chambers are so tight, he has to proceed with 2 punctures. The second puncture takes several tries, because sub-clavian artery and thoracic duct are hard to discern from subclavian vein. Watching Dr. Tu tirelessly try repeated, I learn how immensely more complex and challenging live operations are compared to textbook protocols.

Layers of scrubs, lead armor pieces, hot operation lights, long hours on foot, and repetitive use of upper extremity muscles demand super-human stamina. My feet ache so much that I retire to the watching room in 3 hours and observe the operations sitting in comfortable chairs. Dr. Tu's dedication and endurance is amazing. After successfully embedding the ventricular lead, he begins inserting the atrial lead. This presents another challenge; the second lead intertwines and dislodges the first lead. He backs up the second lead many times, adjusting the shape of the wire and switching to new wires. Some techniques I observe include rotation or jostling while advancing the wires and shaping the wires. I am amazed at his patience. Instead of feeling frustrated, he integrates and executes the advice of many observers (cardiologists, manufacture bio-engineer). At Dr. Tu's request, another cardiologist Dr. Fong enters the operation room for 1 hour to assist atrial/2nd lead insertion. He comes out sharing with us the extreme challenge of the case. Dr. Tu perseveres and finally completes the procedure. My respect and appreciation for dedicated doctors and surgeons like Dr. Tu is beyond words!

We all celebrate and eat lunch in the watching room--Dr. Tu's success. It is such an honor to witness this extremely difficult case. Dr. Chen, the director of Cardiology, says that cases as trying and arduous as this one, present only twice annually. Dr. Chen (Cardiology chief) teaches us about thrombus, embolus, and thrombo-embolus. Virchow’s triad: stasis, hyper-coagulability, and endothelial injury contribute to thrombus. It often happens in prolonged period of immobility and poor flow, like sitting during long flights. Emboli often happen in younger patients, because they are more mobile; likely to dislodge and move fragments throughout the bodies. Venous fragments entering the R heart often are resolved in the lungs. Arterial or L heart emboli often cause more several problems, such as stroke and or digits necrosis. One very special case was a young man with 2.7cm bacterial vegetation on his mitral valve, which sends off septic emboli to the brain, causing cerebral infarction in parietal lobe. He was riding a mopad and experienced left side paralysis due to the cerebral infarction. Thrombo-embolus require thrombogenic AND emoblization conditions, so it’s rare. Deep vein thrombosis often throw small clot into the lungs through the R heart. Healthy lungs resolve them easily.

After lunch, Dr. Chen (CV surgeon) performs two procedures, both on dialysis patients. One patient has stenosis in her endogenous shunt, so Dr. Chen inserts a balloon angiograph. He takes a radiograph of the vessels with contrast, which show two major areas of stenosis. After lidocaine location anesthesia, he punctures the graft and inserts the guide wire. He then uses the bones as landmark for placing the balloon at the stenotic area. As the balloon inflates, he watches closely. Two major principles are: the middle of the balloon exerts maximal pressure on the vessels; the areas inflate the slowest or even forces the balloon to slide away (forward or backward) are the most rigid/problematic area. This vascular responsiveness to the balloon inflation also represents vessel compliance. If an area has extremely low compliance, one should be weary of a higher risk of rupture. After several balloon inflations at the two steonic areas, Dr. Chen checks with contrast imaging. The vessel looks smooth and beautiful. He also teaches us how to distinguish acute thrombus from chronic ones. Clinically, acute thrombus present with 5 P’s: pain, pulse-less, parasthesia, pallor, and poor flow. In angiography, chronic thrombus will present with well-developed collateral circulation, which have high flow and cover wide area. Acute thrombus will stop acutely with weak flow through tributaries.

The 2nd case was a completely occluded graft shunt. Dr. Chen opens the artificial vessel with a 1 cm incision. He uses suction to drag clot out; fresh ones are redder then the harder more organized thrombus. He also injects saline through the cut, towards both arterial direction and venous direction, alternating flushing with suctioning. After meticulously suturing the vessel back, he checks the lumen with contrast.

This concludes my day of many firsts: scrubbing in, wearing lead suits, observing pace maker insertion, hemodialysis shunt balloon angioplasty and open-vessel thrombus removal. Days, months, decades like today is truly not for the faint of heart!

I heart this!

Surgical Department Meeting 8-9am

The surgical chief held a discussion on adjusting the surgical department schedule. It was interesting to observe the interactions between the various sub-specialty surgeons. There were 3 residents, 2 males and 1 female. After roughly half an hour, there was a surgical ultrasound presentation by the manufacture representative. Along with surgeons we learned about the various ultra-sound probes, as many as 20. It's amazing how much instrumentations can enhance the accuracy and precision of medical procedures. The probes have varying ranges of frequency. The higher frequencies are more energetic, causing more rapid tissue reaction, therefore the resolution is higher. However, higher frequency wave can't penetrate as much. So the surgeon can adjust the probe frequencies according to the procedure and the organ/tissue densities. Another important thing mentioned was CIDEX, the agent for cleaning U/S probes. It is a known carcinogen. So the representative recommended having a separate room for CIDEX related cleaning. The probes will not withstand high temperature high pressure sterilization.

U/S, EKG lab 9-12pm, 2-330pm

Dr. Chen performed several cardiac U/S today. A 60 year old patient had an ASD surgically repaired 4 years ago; the echo showed no sign of R atrial dilatation. The patient had 80% LVEF (left ventricular ejection fraction). Dr. Chen said that most of the time >55% LVEF is considered normal, but one must pay attention to the other parameters as well. For instance, LVEF can be easily distorted be MR (mitral regurgitation). LVEF is the difference between ESV and EDV divided by EDV. So if blood is flowing backwards into the atrium during systole, ESV would be lower than if the patient did not have MR. In addition to an incorrectly low ESV, the EDV may also be incorrectly high. This is because the retrograde blood into the atrium during systole in MR adds to the returning venous blood upon subsequent ventricular filling.
Hence, moderate to severe MR often renders an erroneously high LVEF, with the increasing EDV-ESV gap. So when the patient’s heart is compensating for the MR, she may have a LVEF of 80%. Taking the severity of MR into account, the true LVEF may be just 60%. When this same patient later on presents with 60% LVEF, her heart is likely in decompensation, early heart failure. The effect of mitral regurgitation on LVEF teaches me the crucial lesson that, “patients are individuals, not numbers.” While epidemiology and statistics are helpful in generating differential diagnosis, as a future physician, I will be taking care of people with unique constellations of symptoms and signs.

Another patient’s chest X-ray showed extremely large cardiac outline. The U/S revealed pericardial effusion. Her heart was function perfectly in spite of the effusion, which hints that the process had been chronic and gradual. If pericardial effusion were acute, the heart would not have been able to compensate and may present as cardiac tapenade. Dr. Chen asked us for some pericardial effusion ddx. We proposed inflammation, caused by infection or autoimmune diseases. We also asked if drugs like doxorubicin can induce pericardial effusion; Dr Fong said that chemo-induced pericardial effusion is common. He also said that nephrotic syndrome, with hypo-albunimia could cause pericardial effusion as well.

We went to the EKG lab and observed EKG and spirometry procedure. The technician was very efficient. Even Sandy and I got our souvenir EKG readings! In Taiwan, the cost for EKG, paid by the National Health Care Insurance is 100NT, roughly 4 US dollars. No wonder so many people get their annual physical exam in Taiwan.

Dr. Chen also explained to us how the tread-mill stress test is done. He uses the BRUCE protocol. The goal is to get the patient to exercise with increasing workload until 90% of expected heart rate is achieved. The age adjusted expected maximum heart rate is 220- Age. Sequential EKG is taken until the end HR is achieved or the patient can’t continue exercising anymore. ST segment depression more than 1 small box renders a positive stress test for angina. However if the R point and J point (beginning of ST) are on the same level at high stress load; they form a normal change of EKG during exercise, a U shape.

He also mentioned that only 10% of the patients referred to him by other doctors are true cardiac cases. Many chest pains were not caused by angina. He said that there were very few physical signs for angina and the chest X ray can not pick up transient ischemic changes in the heart either. Careful history taking is the best way to rule out non-angina chest pain. He then can follow up high-risk angina patients with stress test. If the stress test is positive, considering 30% are false positive, he often recommends pharmacological management. Unless the patient wants to ensure anatomically definitive diagnosis, or the patient refuses to take medication, Dr. Chen often don’t advise patient to receive coronary angiogram. When performed, angiogram is the gold standard for CAD, specifically coronary artery stenosis.

ABD U/S 330-500pm (Pediatrician Dr. Wu)

On average, Dr. Wu performs abdominal U/S in 5 minutes. He checks liver, spleen, GI, kidneys and pancreas. Many patients present with ascites, most of them due to liver cirrhosis. I noticed that they all had gingival bleeding; Dr. Wu explained these patients suffer bleeding tendency due to lower level of clotting agents. One of the ascites patients did not have liver problem, so Dr. Wu said either the kidney or the heart could have underlying diseases. He said it’s very important to determine the etiology of ascites. He also explained the fundamental principles behind U/S. Solids are more echogenic than fluid. The U/S wave easily transmits through blood and water without bouncing back, and therefore appears black on the sonography. Air, is very interesting, I thought originally that it is less dense than water, it will be completely non-echogenic. But gases are actually highly echogenic because they compress and oscillate, emitting unique echo.

We saw many cysts and nodules, hepatic and renal. One case of hepatic carcinoma; there was a central nodule surrounded by peripheral tributary nodules. Midler cases include alcoholic liver/fatty liver, ileus/ABD fullness. One case presented dilated renal pelvis so we searched for obstruction of the ureter. Because ureters run retro-peritoneal, it was unlikely that stool impaction caused the obstruction. Only ascending or transverse colon impaction could potentially block the ureter; but fecal impaction is usually more distal, in the colon or rectum. So the renal pelvis dilation was most likely caused by kidney stone obstruction.

Several patients had GB sludge or gallstones. Dr. Wu showed us some images from Endoscopic retrograde cholangiopancreatography (ERCP). He was able to remove small gallstones one by one through ERCP. There was a case of pneumobilia, air in the billiary duct. Potential etiology included gas-producing bacterial infection, biliary-enteric anastamosis, an incompetent sphincter of Oddi or biliary-enteric fistula.

Evening outpatient clinic 6-8pm Dr. Chen (Oncologist)’

We had a few patients. Dr. Chen consulted a patient with negative-EGFR-mutation lung adenocarinoma at great length. In their discussion, much of the pharmacology, management plan, recent oncology research Dr. Chen shared with us via powerpoint presentation last week came together. His ability to address difficult cases by thinking quickly on his feet stems from his continual and well-rounded education. He is extremely keen on current research and constantly tries to expand his knowledge base to include more skills (eg. Acupuncture, TCM) to improve patients’ quality of life. When there was downtime, Dr. Chen showed us how he applied acupressure stickers to patients’ ears to support weight loss. Borhan and I volunteered to receive similar treatments. Dr. Chen also observed our individual needs and applied acupressure stickers to locations on our ears accordingly. For instance, he used a point to balance my sympathetic and parasympathetic tone. It was very fun. We also reviewed some of the acupoints Dr. Chen taught us last week. He even asked us to try locating the points on his patients.

Matters of the Heart

Internal medicine meeting 8-9am

Case was an elderly patient with ischemic bowl disease. Pt had a history of CKD and Hypertensive heart disease. The systemic vascular disease led to ischemia, infarction, and ultimately necrosis. Bowl bacteria invaded in the intestinal veins and traveled into hepatic portal vein. The CT scan showed branching pattern of blackness through out the liver. I have never seen that before. It turns out to be bacterial gaseous byproduct, filling the hepatic vascular bed with gas. The attending informed the family that the mortality was 100% without operations, but mortality surgically removing the majority of small intestines will be 80%. The family opted out of the operations. One of the nephrologists led us in several interesting discussions about the intricacies of using diuretics on edematous patients. There are several pathophsyiology behind edema. For pulmonary edema, it's usually due to L heart failure. Using diuretics in CHF patients is tricky in that over-diuresis can lead to insufficient preload, decreasing Frank-Starling contractility. So for CHF, beta agonist is often used in conjunction with diuretics to ensure that contractile force and heart rate compensate for decreasing filling pressure. For LE edema and ascites, it is often due to liver cirrhosis or nephrotic syndrome. So it is likely that the effective circulating volume is higher than normal. Although often dropping oncotic pressure (due to proteinuria-induced-hypoalbuminia) can cause intravascular fluid shift into ECF, the kidney insufficiency also lead to water and sodium retention. So for chronic kidney disease, loop direuetics are the most effective, and there's less concern for hypovolumia with fluid reduction tx. For liver cirrhosis, decreased liver production of protein also reduces oncotic pressure; the other major pathophsyiology is venous flow back up. This will present with ascites and LE edema, and fluid overload as the body try to compensate for lack of arteriole blood volume. As Dr. Lopes so eloquently pointed out last semester, "fluid volume needs to be at the right location; venous blood backed up due to liver cirrhosis is not useful for perfusing the rest of the body."

A cardiologist also brought up different ways to monitor intravascular volume. Echocardiograph is non-invasive and very effective. One can check the diameter of the IVC, returning blood from the liver to the right atrium. If IVC is engorged, then there's fluid overload; if IVC collapsed, it's hypovolumia. Another more invasive constant monitoring is to measure central venous pressure.

We are curious if the massive amount of air in the hepatic vascular bed caused air emboli. Attending Dr. there were no clinical signs of emboli. The patient died, within 4 days of admission, of dropping BP and inoperable bowl infarction. We reasoned that the BP decrease due to septic shock even though the patient was too fragile to mount a typical systemic bacterial infection fever prior to shock.

Cardiology outpatient clinic with Dr. Chen (Department chief) 9-10am

We saw nearly 15 patients. Dr. Chen provides consultation on TLC, blood pressure/sugar control, and side effects management, choice and switch of medicine.

Cardiology rounds (3 cases) 10-11am
One case had aortic stenosis; I could hardly hear the systolic murmur in the room. But this made me realize that the ward is a fantastic place to practice my physical findings skills!
Another patient is 92 years old. She has complete AV block, grade III, ventricles and atria are marching to their own bands. Dr. Tu recommended PCI of setting up a pace maker for her. Sandy and I may be able to observe the procedure, yay!
The last patient was admitted due to UTI, Klebsiella pneumoniae. She was treated w/ Cefazolin; however he also suffered from HTN, CHF, and hypoglycemia. Dr. Tu stopped her glucose lowering meds. She was on both ACE-I and spironolactone. This is because long term ACE-I use will cause up-regulation of aldosterone receptor to compensate for reduced RAAS production. Spirolactone blocks aldosterone receptor and works in synergy with ACE-I. Getting to know a patient and his multiple drug list to manage intertwined co-morbidities is the best way to learn pharmacology!

Echocardiography 11-12pm, 2-5pm

We were in the ultrasound lab for several hours in the morning and in the afternoon. It was a fantastic review of some of the concepts we learned in CVRR and wonderful expansion of our currently knowledge base. Many of the patients had mitral regurgitation, but mostly mild cases. We learned to identify MR on the echocardiography. First locate the central of the valvular closure, then look at the color of the Doppler map. If there is a high frequency jet, then it is likely regurgitation. Because valvular insufficiency is similar to a slightly cracked open door, so when blood flows back through the crack, it'll be high velocity. We also learned concepts like QP/QS (pulmonary flow/systemic flow); normally, the ratio is roughly 1. However, if there is shunting, QP/QS may be greater than 1. For instance, in VSD, blood is shunted from the L side to the R due to the higher pressure in L ventricle. This will increase QP, simultaneously decreasing QS. We saw a case of mild para-menbranous VSD with incidental discovery at age 42.

Another case was really sad, a man in his 50s with H/O severe hypertension was experiencing tremendous stress at work; he was a security guard manager. One day he went to bed anxious about multiple phone calls from work reporting bad news, his middle cerebral artery ruptured. By the time his wife rushed him to the ER, 70mm of hemorrhage had been pressing on his brain. He had emergency craniotomy to remove the hemorrhage. But a couple hours later, another major artery ruptured in his brain. The trauma left him non-verbal and bed-ridden. In the matter of 7 months, he developed severe bed sore, to which repeated skin graft was rejected and detached. He now has a enormous raw spot on his buttock. He also has 3 tubes inserted, nasal-gastro-intestinal tube, fecal tube and urinary catheter. It is heart-breaking to see the condition he is in. His wife has been taking care of him since the traumatic events. I really admire her.

We also reviewed EKG. We saw a case of torsa de point. The earlier EKG strip showed warning signs of TDP, QT prolongation, which is a contra-indication for Amioderone. The cardiologist explained to us that there are 3 ways to salvage QT prolongation: Lidocaine, adminster K if hypokalemia was the cause, and beta agonist. He said that lidocain is a class Ib anti-arrthymic drug which shortens action potential by blocking Na channels. Beta agonist can also shorten action potential by increasing sinus beats. Correcting hypokalemia will also allow myocyte to depolarize more easily, increasing heart rate. We went to the ICU to check on the TDP patient; the doctor emphasized that we must switch the patient away from amioderone, as it shows both beta-blocker and K-channel blocker effects, worsening QT prolongation and TDP. Although the staff d/c Amioderone last night, they still had to defibrillate him many times due to the extremely long half life.

Other EKG features we saw were RBBB, hemiblock, L anterior fasicular block and posterior fasicular block. It's great to apply what we learned from Dr. Lope's narrated powerpoint and lab discussion real time. Dr. Tu showed us how to determine posterior from anterior fasicular block. In lead II, III, F, if the biphasic showed predominantly positive, then it is posterior fasicular block. If the biphasic ventricular QRS wave was mostly negative, then it is an anterior fasicular block. We also learned to identified and qualified locations of hyperkinesia, hypokinesia, dyskinesia, and akinesia. He said that with each contraction, the ventricular wall thickens, and then relaxes into a thinner configuration. If we see asymmetry between two ventricular adjacent to each other, the side that demonstrate lower amplitude in thickness changes is hypokinetic. This is often due to prior MI; if the MI is very severe, then the area can become akinestic (does not contract at all). Also, when one part of hear is hypokinetic or akinetic, the rest of the heart may compensate with hyperkinesia. Lastly, damaged myocyte that healed with fibrous cap becomes a ventricular or atrial aneurysm, which is dyskinetic, means that it has paroxysmal movement, bulging out when the rest of the healthy heart wall contracts. We saw a case of elderly patient, who had global hypokinesia, with severely compromised ejection fraction.

On the note of decreasing ejection fraction, I asked about what is the minimum EF that requires surgical intervention. Dr. Tu said that some virus and medications frequently cause dilated heart disease, leading to patients with 10-20% in EF. I read more about EF tonight and realized that EF can be increased with medications and mild physical therapy, life style changes, etc.

Pacemaker wound infection, case maker removal operation/wound cleaning 5-6pm

Dr. Fong, the cardiology director shared his experience of managing cardiologist patients; he also consulted us on as Dr. Tu inspect a patient’s mitral valve prolapse with U/S. They mentioned a cardiovascular surgery about to take place; Sandy and I were both excited. So I asked if it was possible for us to observe the procedure. Dr. Fong graciously made a phone call for us and took us to the operation room himself. The cardiovascular surgeon welcomed us warmly. Nicole is rotating with the CV surgeon this week, so we joined her. It was a fabulous experience. Even watching the surgeon scrubbing and dressing methodically prior to the operation was an eye-opener. He administered local Lidocaine 30-60 seconds prior to the first incision. He used an electric cauterizer, gingerly he extended the opening of the pacemaker horizontally. His goal was to remove the pacemaker and apply wet dressing to the infected, purulent wound. As soon as the patient verbalized pain, the surgeon dexterously injected additional Lidocaine, comforting the patient and then resuming excision. His plan is to apply wet dressing for a week while sterilizing the pacemaker, and then reinsert the pacemaker after infection is cleared. To insure better healing and reduce infection risk, he said that he will make a deeper pocket to house the pacemaker. Contrasted with the shallow pocket of the original pacemaker placement, this will reduce the tissue tension and promote wound healing. He emphasized that post-op healing should be one of the surgeon’s priorities, “you can be very good in surgery, but if the post-operation recovery is poor then you have mostly failed.” That ringed in my ears, resonating with “Do no harm.” At last, we asked if it is possible for us to observe the other 2-3 procedures scheduled during this week, he replied genuinely, “Any time! You can come here to learn anytime you’d like.”
After inspecting the heart in numerous ways today: from listening to heart murmurs in hospitalized patients, observing outpatient CV consultation and CV surgery, to echocardiograph, EKG, and chest radiograph, I am truly amazed at the enormity of each heart around me. Dr. Tu tirelessly answers my questions about CV epidemiology, pathophysiology, and pharmacology while performing U/S and attending to his patients; Dr. Fong support us beyond 8-5 schedule to learn; the CV surgeon welcomes us to observe the pacemaker extraction and wound cleaning. I am grateful and honored to learn from such big-hearted individuals.

“Nobody has ever measured, not even poets, how much the heart can hold.”
----Zelda Fitzgerald

The extraordinary in the ordinary

Internal medicine meeting 8-9am

Case 1: We followed up with yesterday's case--unconscious alcoholic with hypovolmia and electrolyte imbalance. Lumbar puncture showed gram + cocci, which most likely was streptococcus pneumoniae. The CSF fluid also showed other signs of bacterial meningitis--high CSF pressure 23 (normal range is 9-18), low glucose level (bacterial consumption of glucose), high WBC count. If it were viral CNS infection, the CSF would have normal CSF pressure, normal glucose level, and possibly high protein level.

There was also RBC in the CSF, so the attending asked the resident for ddx from gross examination. If an elevated number of red blood cells is present equally in all bottles, this indicates a subarachnoid hemorrhage. If the number of cells decreases per bottle, it is more likely that it is due to damage to a small blood vessel during the procedure (known as a "traumatic tap"). CSF also had RBC (normally found in CSF)--its presence indicate bleeding; ddx are subarachnoid hemorrhage, stroke, or traumatic tap. We've ruled out traumatic tap with the resident's observation, how to discern stroke from cerebral hemorrhage? Since WBC may enter the CSF due to infection (viral, bacterial, fungal, and parasitic), allergy, leukemia, hemorrhage, traumatic tap, encephalitis, and Guillain-Barré syndrome, the RBC count is used to correct the WBC count. WBC corrected with RBC will help determine if the CSF display merely bleeding conditions. If the RBC to WBC ratio of CSF is similar to that of patient's blood, then we can conclude that the tainted CSF (elevated RBC, WBC)was caused by bleeding. But if the ratio is dramatically different, with WBC/RBC ratio much higher in CSF, the etiology is mainly infectious. It's incredible how much information and analysis rest within a seemingly ordinary procedure such as lumbar puncture!

Another interesting point was that with bacterial infection, neutrophils is most likely elevated. However, the CSF sample showed elevated lymphocytes. I was thinking perhaps it was a super-infection (both bacterial and viral) or a chronic infection with acute presentation (meningitis). The attending said that it could be a TB infection transitioning from acute to chronic course, which would have a higher percentage of lymphocytes than most other bacterial infection.

He then emphasized how imperative it is to determine the etiology of meningitis: bacterial, viral, fungal, or parasitic. With bacterial meningitis killing people in matters of hours to a few days, doctors can not risk to prescribe the wrong category of treatment. It is very rare to administer antibiotics, antiviral, and/or antifungal simultaneously, so the clinical picture and preliminary lab results must help decide the pathogen. Unfortunately, even with the diagnosis of bacterial meningitis and Penicillin G/Vancomycin/Ceftriaxone, our patient died of septic shock.

We also discussed 2 new cases. I hope to meet and interview these patients. Will propose this to Yu-Yu.

Chinese medicine acupuncture 9-11am
Acupuncture-CINV 2-430pm

Dr. Chen taught us 10 major acupoints. He said the ultimate goal is to enhance and optimize the flow of Chi. The points were mostly on our upper and lower extremities; knowing our anatomy was quite helpful in locating the points. He explained that each acupoint is analogous to the station of the rapid transit, leading to acupoints upstream and downstream of itself along the transit line. This is the basis of how an acupoint on the anterior leg can affect bowl movements and reproductive health. The techniques go beyond accurately locating the acupoints, which vary from one person to another based on primarily size. They include swiveling the needle, pulling the needles in and out, depth, and angle. The introduction to principles of acupuncture correlated well with several osteopathic principles. Some acupoints resemble counter-strain points; others resemble Chapman’s points. It'd be very exciting to share what we learn from Dr. Chen with the OMM department and our class in the fall! Dr. Chen agreed to let us shadow him during his evening outpatient clinic on Tuesdays, just need to clear with TIHTC. This may open doors to our shadowing other specialty doctors in the evening clinics across the board, including OB/GYN, pediatrics, cardiology, and surgery.

Pathology review of Colon Cancer section from yesterday 11-12pm

With the teaching microscope, 5 of us had a tour of the slides prepared from the resected colon tumor. We started with the normal tissues and contrasted that with the malignant ones. The latter showed loss of polarity, disorganization, disproportionate cell type, invasive behavior, and invagination into glandular lumen. She also showed us the lymph nodes from the serous layer of the colon. Fortunately the nodes displayed beautiful germinal centers without glandular invasion. She also briefly reviewed the cancer staging system of TNM (tumor size, lymph node involvement, and distant metastasis). Finally, she recommended the framework for our case presentation.

Dean: organize power point, host and direct and case presentation
Family physician: prepare, present epidemiology, H&P
Surgeon: prepare, present operational findings, course of hospitalization
Pathologist: prepare, present pathology findings/diagnosis
Oncologist: prepare, present out-patient treatment--chemo, and or radiation
Chinese Medicine Doctor: prepare, present adjunct, supportive therapy
Students: prepare and ask questions

Her gracious guidance is heart-warming and inspiring. Jessica, Borhan, Mickey, Sandy, and I are quite excited about this project. We would love for Karen and Nicole to participate as well--we especially need good questions at the end of the presentation. Dr. Hsieh has already invited big shots including Superintendent Lin to grace our 1 hour case presentation happening in 2,3 weeks!

Neurology conference--Adverse Drug Reaction of Anti-epileptic Drugs 1230-2pm

Case 1: phenytoin intoxication
Patient had liver and renal insufficiency. Phenytoin has zero-order kinetic. Patient was not able to metabolize/deactivate the phenytoin prescribed. Hence she suffered altered consciousness. After admission, neuro-surgeon reduced and ultimately discontinued phenytoin.
Clinical Pearl: Start low, go slow (Monitor serum drug level for metabolically compromised patients) Dr. Lin taught us take caution with renal or hepatic insufficiencies last fall!

Case 2: Stevens-Johnson syndrome with carbamazepine
A study with 44 East Asian subjects showed that all patients w/ SJS had HLA-B*1502. So physicians could prevent SJS by taking careful PMH and FH and genetic testing for HLA-B*1502 before using carbamazepine and phenytoin in high risk population. However, genetic testing costs 3000NT while carba. oral costs only 2-3 NT dollars, so the national health insurance refuse to pay for the testing. The presenter pointed out that often once SJS presents with rashes and blisters, nearly 50% of patients will die from it. It is unclear if discontinuation of the inciting medication can stop the course of severe inflammation. We also learned to distinguish TEN (Toxic epidermal necrolysis) from SJS. SJS distributes throughout the body diffusely while TEN concentrates on the chest and neck; SJS normally involves 2 or 3 mucosa: oral mucosa, conjunctiva, and genital area.

Amputated man in the hall

I rode the elevator with a man yesterday. His painfully deformed gouty finger joints burned a vivid image in my mind. I felt so sad to see it. Debilitating diseases we learn on paper and in discussion happen to REAL people. Today I recognized that same man in the hall, lying on a gurney. He looked so sad and life-less. I took another glance at him and realized that his short stature was due to bi-lateral above knee amputation. A wave of sadness grabbed me; I tried to share this with my colleague as if somehow we could commiserate--somehow I can take comfort in finding others who feel the same shock. One colleague thought positively, "At least he had a whole life ahead of him. We can focus on being thankful that he is not dead." Another colleague said, "but how about quality of life? Disabled, poor, and possibly with less disability support/ infra-structure than in the States. How good can his life be?" Both view points are valid. Caring for those who have survived severe life-changing medical conditions is an important lesson to for us to learn.