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.
Showing posts with label Nephrology. Show all posts
Showing posts with label Nephrology. Show all posts
Sunday, July 10, 2011
Tuesday, June 28, 2011
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.
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.
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