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Medicine by Alexandros G.Sfakianakis

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Τρίτη, 3 Ιανουαρίου 2017

Post-traumatic pituitary apoplexy



Volume 7, March 2017, Pages 4–8
Open Access
Case Reports & Case Series (CRP)

: Case presentation and review of literature


Highlights

Head trauma could be a non negligible risk factor for pituitary apoplexy, with frequently the occurrence of a consistent delay from trauma to apoplectic event. Furthermore post-traumatic PA can be misdiagnosed with other neurological syndromes (SAH, meningism).
Even after a mild head trauma, head MRI scan should be performed in case of upper cranial nerve deficits or neurological deterioration even if head CT scan documented a sellar mass without signs of haemorragic / ischemic events.
Elderly patients, especially under anticoagulants/antiplatelets agents, with a medical history of pituitary adenoma should be aware about the risk of late ischemic/haemorragic events.
In case of post traumatic PA with acute and progressive neurological deficits trans-sphenoidal endoscopic decompression should be, if feasible, a mandatory treatment.

Abstract

Pituitary apoplexy is a dramatic condition that can occur spontaneously or triggered by various precipitating factors. Head trauma is a rare but well-recognized cause of apoplectics events. We present the case of an 81-year-old woman, with negative past medical history and under antiplatelet agents, who experienced an isolated VI cranial nerve palsy 24 h after a mild head trauma. Early brain CT revealed an unknown pituitary lesion without signs of intralesional bleeding. Only late brain MRI imaging revealed pituitary apoplexy together with a subarachnoid hemorrhage. After aggravation of neurological condition the patient, undergo endoscopic transsphenoidal decompression of cranial nerves with rapid deficits improvement. Our aim is to share our experience and to propose the first critical review of all cases of post-traumatic pituitary apoplexy described in literature. We also try to suggest some management advice for post traumatic pituitary apoplexy.

1. Introduction

Pituitary apoplexy (PA) is a rare event characterized by a rapid expansion of a pituitary adenoma after a hemorrhage or ischemia, and occurs in about 14–22% of patients [1]. Male-to-female ratio is 2:1, and most cases present in the V or VI decades of life [11]. PA is a dramatic condition that can be sometimes life threatening for the patient [9]. 70–81% of patients with PA had negative medical history for pituitary adenoma [9] and [15]. PA can be asymptomatic and recognizable only after performing neuroimaging, and is therefore called subclinical or subacute apoplexy [14]. Pituitary adenomas can develop silently, enlarge and then suddenly become symptomatic after triggering events such as head trauma, radiation therapy, sudden changes in intracranial pressure, dopamine agonists administration, hormone stimulation tests, lumbar puncture or spinal anesthesia [1][5] and [13]. Some authors argue that pituitary apoplexy is more prone to occur in large pituitary tumors (e.g. macroadenoma) whereas microadenomas (< 1 cm in diameter) are less susceptible to bleeding [14]. Studies showed than about 70% of pituitary apoplexy occurred in nonfunctioning adenoma [10] and [15]. Furthermore, there is no evidence that a defined histological type of pituitary tumor is more susceptible to apoplectic events [3] and [15].
To date, only 12 cases of post-traumatic pituitary apoplexy are described in literature. In this report we want to share our experience in the management of post traumatic PA and propose the first critical review of all cases described in literature.

2. Case presentation

We report the case of an 81-year-old woman, which accidentally fell, in October 2015, from about 1.5 m height with subsequent mild head trauma and blunt contusion on her occipital bone. She was under lifetime prophylaxis with antiplatelet drugs. After she was admitted to the Emergency Department she underwent a brain CT scan which highlighted a left frontal contusion with subarachnoid hemorrhage (SAH), together with the evidence of an undiagnosed pituitary lesion (Fig. 1a, b). Neurological examinations were negative. Twenty-four hours later, she developed VI c.n. (cranial nerve) palsy with no evidence of diplopia or visual acuity loss. Visual field defects were not documented on manual visual field testing. A new brain CT scan showed that the pituitary lesion had enlarged in size, with presence of hyperdense foci, signs of potential intralesional hemorrhage (Fig. 1c). Imaging was compatible with pituitary apoplexy. A comprehensive hormone panel was performed which confirmed mild hypopituitarism (Prolactin 1.7 ng/ml, T3 1.93 mIU/ml, serum cortisol 2.9 ng/ml) and brain MRI (magnetic resonance) scan showed bilateral subdural hematoma together with left temporal and frontal contusions as well as an intrasellar-suprasellar lesion, of 30 mm × 20 mm size, with signs of recent bleeding (Fig. 1d). Brain MRI imaging evidenced how the sellar lesion exerted compression on chiasm and optic nerves, which were dislocated. In the first hours after PA diagnosis the only neurological sign manifested was the VI c.n. palsy and, considering patient's age and comorbidities, we adopt a “wait and see” approach. The patient's clinical conditions were constantly monitored and hormone replacement therapy was administered. After 4 days the patient complained of progressive loss of visual acuity (01/10 on right eye (R.E.) and 2/10 on left eye (L.E.)) and temporal hemianopsia was confirmed by Goldman visual field examination. At that point, surgical treatment was mandatory (Fig. 1d, e). The patient underwent endoscopic trans-sphenoidal surgery in order to decompress optic nerves (Fig. 1f). Histological and immunohistochemical examinations showed extensive necrosis with fibrosis and inflammatory granulation infiltration. The lesion express diffusely synaptophysin together with Ki-67 in 3% of cells, whereas ACTH, prolactin, CKCAM5.2, FH, TSH, GH were not expressed. At that point, the pituitary apoplexy was confirmed. After surgical decompression, visual acuity progressively improved. The patient underwent brain MRI imaging that documented a satisfactory decompression of chiasm and optic nerves. Clinical evaluation at 30 and 60 days documented recovery of visual acuity (4/10 in R.E. and 4–5/10 in L.E.) as well as of visual field impairment. Long-term MRI follow-up did not document any further complications (Fig. 1g, h).
Fig. 1
Fig. 1. 
Early after head trauma axial brain CT scan (a) and 6 h later brain CT scans (b); 24 h axial brain TC scan; recognition of pituitary apoplexy and first manifestation of symptoms (c); 36 h later T1 contrast enhanced axial brain MRI scan: aggravation of neurological condition (d) and 48 h later post-apoplexy CT axial scans (e). Postoperative axial T1 contrast enhanced brain MRI axial scans (f). Early (g) and long term follow up T1 contrast enhanced brain MR axial scan (h).

3. Discussion

In 1932 Van Wagenen reported the first two cases of post-traumatic pituitary apoplexy and since 1983 no other cases have been described [2]. In addition, Dr. Harvey Cushing described a similar case in which the pathological examination documented a pituitary tumor with extensive blood infiltration in a patient died after head trauma [2]. In our review of literature, including our case report, we identified 13 post-traumatic pituitary apoplexy cases from 1983 to 2016 (Table 1). 9 patients were men, with a male to female ratio of 2:1, which is also the reported ratio for PA in literature. Age ranged from 30 to 85 with a mean age of 58.7 years. All patients were unaware of the presence of the pituitary tumor. In 2 cases patients complained of symptoms compatible with GH over secretion and in one case symptoms of increased serum prolactin levels were manifest.
Table 1.
Literature review summary of post traumatic pituitary apoplexy.
AuthorsAge (years)SexMedical historyDynamics of traumaDelay (time)SymptomsImagingTreatmentPost-operativeHormonal replacement therapyFollow up (months)Antiplatelet medications
Haruaki U et al. [4]199960FXFell down stairs with occipital trauma1 hLethargic, VI. PL on RE, MM on LECT + RMTSS + TSSRIX1n.d.
Haruaki U et al. [4]199966MXFell from a 4-m-height with back trauma15 hLethargic, MMCT + MR: pituitary apoplexyCTRIX4n.d.
K. Kayayurt et al. [1]201568MXFell with occipital trauma2 hOPMR: pituitary apoplexyn.d. (surgical)OPYes3X
Ravi Dev et al. [3]200740MXHead-on collision of motorcycle with a road divider7 hMM in RE; 2/10 in LE; hemianopsiaCT: hematoma in sella and supra-cellar region + hematoma in the basi-frontal regionTTS2.5/10 in RE, 5/10 in LE, hemianopsiaXn.d.n.d.
Horie N et al. [12]200256FXTraffic accidentn.d.LethargicMR: pituitary apoplexyFronto-temporal CTNoXn.d.n.d.
Itoyama Y et al. [7]199945MXFell from a 2 m height with right frontotemporal trauma3 hAnisocoria, OP, VI hemianopsiaCT: SAH due to pituitary apoplexy AGF: vasospasmsNST7/10 in RE, 3/10 in LEYes> 27X
Holness RO et al.[2]198339MXHead injury with fracture of right patella< 1 h1/10 on LE; MM on RE, hemianopsiaCT: pituitary apoplexyFrontal CT + RTMild recovery on LE. 5/10 RE, hemianopsiaX3X
Smidt MH, et al. [6]200730MXFell of a truck3 wOP, 5/10 RE; 8/10 LECT + MR: pituitary apoplexyTTSRIYes5n.d.
Lin Chang et al. [11]200985MXFell, minor parietal trauma6 dHDMR: pituitary apoplexyNSTRIYesn.d.Yes
N. Tamasawa[8]198834MXFell from the back of a truck2 dVICT: no pituitary apoplexy RM: signs of hemorrhageNSTRIYes2n.d.
Mohammad Sami Walid et al. [5]200980FXFell in the yard< 1 hNo VICT + RM: SAH due to pituitary apoplexyNSTRIYes48Yes
Bao Xi ling et al. [9]200779MXFell, head occipital trauma6 hNo VICT + RM: SAH due to pituitary apoplexyNSTHDYes18n.d.
Present case201581FXFell from 1.5 m height + occipital trauma24 hOPCT + MR: pituitary apoplexyTSSRIYes6Yes
Legend: VI: visual impairment; HD: hormonal deficits; RE and LE: right and left eyes respectively; OP: ophtalmoparesys; NST; non surgical treatment; TTS: transsphenoidal surgery; CT: craniotomy; RI: restitutio ad integrum; MM: motu mano; PL: perceive light; SAH: subarachnoid hemorrhage; AGF: intracranial angiogram; X: no.
To date the pathophysiological mechanism underlying post traumatic pituitary apoplexy has not been established [4]. The pituitary gland is perfused by its portal venous system, which passes down the hypophyseal stalk. It is well described how the particular pattern of vascular supply contributes to the occurrence of pituitary apoplexy [3]. Dandy et al. suggest that pituitary massive hemorrhagic infarcts can be consequent to traumatic shearing forces that cause the destruction of the pituitary stalk and lead to the consequent blockage of pituitary portal vascularization [2]. Several authors support that if the trauma involves the occipital region, as occurred in 9 cases (Table 1), shearing-rotational forces are more susceptible to tear the fragile junction between the intra-sellar portion, that is relatively firm, and the supra-sellar portion, that lies freely within the supra-sellar cistern [1]. Others authors argue that after a head trauma an intralesional hemorrhage can occur, such event alter the venous vascularization pattern encouraging ischemic-hemorrhagic occurrences. This hypothesis can explain the delay in post-traumatic PA onset and symptoms manifestation[4]. Other authors suggest that also, arterial vasospasm may have a role in post-traumatic PA, but the pathophysiological mechanism have still to be clarified [3].
It is well known how anticoagulants and antiplatelet agents, especially in elder patients, can facilitate and worsen adverse vascular events. After head trauma, owing to anticoagulant/antiaggregant therapy, small bleedings that should be silent turn instead into massive ischemic-hemorrhagic events, as described in 3 cases (Table 1[6].
Most common symptoms of PA are headache (63–100%) [10] and [15], nausea (80%) [10], vomiting (20–77%) [15], visual acuity deterioration (56–75%) [10] and [15], ophthalmoparesis (45–68%) [15], hypopituitarism, dizziness, confusion and even coma (13–77%) [10] and [15]. Symptoms may have an acute or delayed onset with a wide variability of clinical manifestations. In 43% of PA cases, involvement of multiple cranial nerves (c.n.) was described. The III c.n. is the most frequently affected, followed by abducens nerve (VI c.n.) in 5% of cases [1]. Hypopituitarism occurs in 70% to 80% of patients and usually becomes persistent, necessitating lifetime hormone replacement therapy [10] whereas diabetes insipidus incidence accounts for 4% for transient and 2% for persistent deficits [8]. ACTH (adrenal) deficit become manifest in 67% of cases, TSH (thyroid stimulating hormone) deficiency in 45%, gonadal hormones in 82% and PRL (prolactin) in 26% [15]. The most dangerous consequence of pituitary apoplexy is sudden death, attributable to the onset of acute adrenal insufficiency [10].
PA symptoms usually become manifest after few hours, with a mean delay of presentation of 14 days, whereas in some cases even 2 months. In the reviewed series of post-traumatic apoplexy, the mean delay after head trauma was 11 h, with in 2 cases a delay of six days and 3 weeks (Table 1).
PA could be misinterpreted as bacterial meningitis, subarachnoid hemorrhage, viral meningo-encephalitis or migraine, [6] and [11] as occurred in 2 of reviewed cases. The high temperature in consequence to PA could be referred as a sign of infections, but is in fact a typical finding in patients with PA. Furthermore ophthalmoparesis, a frequent sign of PA, can be wrongly referred as ocular motility disturbances associated with meningitis. It is therefore advisable to mind about the possibility of pituitary apoplexy when mental alteration and meningismus appear together, even without visual or other cranial nerve deficits [11].
A full clinical and instrumental diagnosis requires adequate neuroimaging, a complete ophthalmological examination, and a full hormonal panel [10]. Head CT scan represents the gold standard for head trauma but CT imaging can highlight a PA only in 25–28% of cases. It is well known that pituitary adenoma, which is isodense to brain parenchyma, is difficult to diagnose on CT even in case of hemorrhage. In the reported cases series CT scans failed to recognize post-traumatic PA in 6 (50%) of cases [1][4][6][8][9] and [11].
Brain MRI imaging is more sensible and allows recognition of PA in nearly 100% of patients[1]. In the suspect of PA, MRI imaging should be preferred.
Sometimes post-traumatic PA accompanies subdural hematomas, as occurred in 4 cases[7] and [8]. In one case of post traumatic PA arterial vasospasm occurred as consequence of SAH, in that case the author suggest to perform cerebral angiography when patients with pituitary apoplexy exhibit rapid neurological aggravation [7] (Table 1).
The combination of endoscopic trans-sphenoidal surgery and hormone replacement therapy is considered the standard treatment in case of pituitary apoplexy [9]. Surgery within the first days is recommended when visual impairments or neurological deficits are manifest, even without acute clinical deterioration. Early surgical decompression is related to an improved neurological outcome. Indeed, patients with progressively improving neurological deficits, particularly with only isolated cranial nerves deficit, could benefit from conservative treatment with subsequent clinical-radiological follow up [10], as we had first intended to do with our patient. If apoplectic events are so dramatic as to be associated with an intra-parenchymal hemorrhage, some authors argue that surgical evacuation can be obtained through endoscopic trans-sphenoidal approach if such hematoma affects the frontal-basal regions, or by craniotomy in other cases [3]. If a surgical approach is chosen, total tumor resection is not mandatory but a prompt decompression of cranial nerves involved is advisable [1] and [8]. In the reported cases series, craniotomy was performed 3 times whereas endoscopic trans-sphenoidal surgery was performed in 6 cases. Four cases were managed conservatively and integration of hormone deficits was administered, with hormone replacement therapy (Table 1). The recovery rate in patients with neurological deficits that undergo early surgery was 73%. This percentage drops to 43% in case of delayed surgery [1] (Table 1).

4. Conclusion

Pituitary apoplexy after a head trauma is a rare event that could manifest acutely or silently with delayed presentation of neurological signs, because of the occurrences of a symptoms-free time interval between trauma and bleeding. Furthermore, pituitary apoplexy does not always show the typical signs of hemorrhage but may also mimic meningitis or subarachnoid hemorrhage syndromes. It is therefore essential for a physician to be extremely cautious in case of elderly patients admitted to the Emergency Department following an head trauma, especially if under antiaggregants/anticoagulants agents, even if they don't exhibit neurological deficits. We suggest performing adequate diagnostic investigations and being aware that head CT scan do not always allow recognition of PA. Furthermore, in case of unexplained neurological deficits, always perform brain MRI scan. It is therefore advisable to warn the patient on potential signs of pituitary apoplexy in case of recognition of unknown pituitary adenoma. As already suggested in literature, we believe that in every case of post head trauma PA case even without acute and progressive deficits (visual acuity deterioration, visual field defects) early trans-sphenoidal surgery through endoscopic route is the mandatory choice for treatment. An accurate recognition and intervention, as described in our case, allows a restitutio ad integrum in most cases and avoid unpleasant consequence for patients.

Conflict of interest

The authors declare that they have no conflict of interest.

Funding

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Ethical approval

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards. This article does not contain any studies with human participants performed by any of the authors.

Informed consent

Informed consent was obtained from all individual participants included in the study.

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Corresponding author at: Department of Neurosurgery, Treviso Regional Hospital, University of Padova, Pzza.le Ospedale 1, 31100 Treviso, Italy.

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Tinnitus

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4. Cannon SC Pathomechanisms in channelopathies of skeletal muscle and brain. Annu Rev Neurosci. 2006;29:387-415. [Abstract]

5. Davies E, Knox E, Donaldson I. The usefulness of nimodipine, an L-calcium channel antagonist, in the treatment of tinnitus. Br J Audiol. 1994;28:125-129. [Abstract]

6. Baguley DM, Jones S, Wilkins I, Axon PR, Moffat DA. The inhibitory effect of intravenous lidocaine infusion on tinnitus after translabyrinthine removal of vestibular schwannoma: a double-blind, placebo-controlled, crossover study. Otol Neurotol. 2005;26:169-176. [Abstract]

Eggermont JJ. Cortical tonotopic map reorganization and its implications for treatment of tinnitus. Acta Otolaryngol Suppl. 2006;9-12. [Abstract]

Hoke ES, Muhlnickel W, Ross B, Hoke M. Tinnitus and event-related activity of the auditory cortex. Audiol Neurootol. 1998;3:300-331. [Abstract]

Mirz F, Pedersen B, Ishizu K et al. Positron emission tomography of cortical centers of tinnitus. Hear Res. 1999;134:133-144. [Abstract]

Muhlnickel W, Elbert T, Taub E, Flor H. Reorganization of auditory cortex in tinnitus. Proc Natl Acad Sci U S A. 1998;95:10340-10343. [Abstract]

Norena AJ, Eggermont JJ. Enriched acoustic environment after noise trauma abolishes neural signs of tinnitus. Neuroreport. 2006;17:559-563. [Abstract]

Schlee W, Hartmann T, Langguth B, Weisz N. Abnormal resting-state cortical coupling in chronic tinnitus. BMC Neurosci. 2009;10:11. [Full text]

Schlee W, Mueller N, Hartmann T, Keil J, Lorenz I, Weisz N. Mapping cortical hubs in tinnitus. BMC Biol. 2009;7:80. [Full text]

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HIPPOCRATE'S OATH

"I swear by Apollo, the healer, Asclepius, Hygieia, and Panacea, and I take to witness all the gods, all the goddesses, to keep according to my ability and my judgment, the following Oath and agreement:

To consider dear to me, as my parents, him who taught me this art; to live in common with him and, if necessary, to share my goods with him; To look upon his children as my own brothers, to teach them this art.

I will prescribe regimens for the good of my patients according to my ability and my judgment and never do harm to anyone.

I will not give a lethal drug to anyone if I am asked, nor will I advise such a plan; and similarly I will not give a woman a pessaryto cause an abortion.

But I will preserve the purity of my life and my arts.

I will not cut for stone, even for patients in whom the disease is manifest; I will leave this operation to be performed by practitioners, specialists in this art.

In every house where I come I will enter only for the good of my patients, keeping myself far from all intentional ill-doing and all seduction and especially from the pleasures of love with women or with men, be they free or slaves.

All that may come to my knowledge in the exercise of my profession or in daily commerce with men, which ought not to be spread abroad, I will keep secret and will never reveal.

If I keep this oath faithfully, may I enjoy my life and practice my art, respected by all men and in all times; but if I swerve from it or violate it, may the reverse be my lot."

MAIMONIDE'S PRAYER

"Almighty God, Thou has created the human body with infinite wisdom. Ten thousand times ten thousand organs hast Thou combined in it that act unceasingly and harmoniously to preserve the whole in all its beauty the body which is the envelope of the immortal soul. They are ever acting in perfect order, agreement and accord. Yet, when the frailty of matter or the unbridling of passions deranges this order or interrupts this accord, then forces clash and the body crumbles into the primal dust from which it came. Thou sendest to man diseases as beneficent messengers to foretell approaching danger and to urge him to avert it.

"Thou has blest Thine earth, Thy rivers and Thy mountains with healing substances; they enable Thy creatures to alleviate their sufferings and to heal their illnesses. Thou hast endowed man with the wisdom to relieve the suffering of his brother, to recognize his disorders, to extract the healing substances, to discover their powers and to prepare and to apply them to suit every ill. In Thine Eternal Providence Thou hast chosen me to watch over the life and health of Thy creatures. I am now about to apply myself to the duties of my profession. Support me, Almighty God, in these great labors that they may benefit mankind, for without Thy help not even the least thing will succeed.

"Inspire me with love for my art and for Thy creatures. Do not allow thirst for profit, ambition for renown and admiration, to interfere with my profession, for these are the enemies of truth and of love for mankind and they can lead astray in the great task of attending to the welfare of Thy creatures. Preserve the strength of my body and of my soul that they ever be ready to cheerfully help and support rich and poor, good and bad, enemy as well as friend. In the sufferer let me see only the human being. Illumine my mind that it recognize what presents itself and that it may comprehend what is absent or hidden. Let it not fail to see what is visible, but do not permit it to arrogate to itself the power to see what cannot be seen, for delicate and indefinite are the bounds of the great art of caring for the lives and health of Thy creatures. Let me never be absent- minded. May no strange thoughts divert my attention at the bedside of the sick, or disturb my mind in its silent labors, for great and sacred are the thoughtful deliberations required to preserve the lives and health of Thy creatures.

"Grant that my patients have confidence in me and my art and follow my directions and my counsel. Remove from their midst all charlatans and the whole host of officious relatives and know-all nurses, cruel people who arrogantly frustrate the wisest purposes of our art and often lead Thy creatures to their death.

"Should those who are wiser than I wish to improve and instruct me, let my soul gratefully follow their guidance; for vast is the extent of our art. Should conceited fools, however, censure me, then let love for my profession steel me against them, so that I remain steadfast without regard for age, for reputation, or for honor, because surrender would bring to Thy creatures sickness and death.

"Imbue my soul with gentleness and calmness when older colleagues, proud of their age, wish to displace me or to scorn me or disdainfully to teach me. May even this be of advantage to me, for they know many things of which I am ignorant, but let not their arrogance give me pain. For they are old and old age is not master of the passions. I also hope to attain old age upon this earth, before Thee, Almighty God!

"Let me be contented in everything except in the great science of my profession. Never allow the thought to arise in me that I have attained to sufficient knowledge, but vouchsafe to me the strength, the leisure and the ambition ever to extend my knowledge. For art is great, but the mind of man is ever expanding.

"Almighty God! Thou hast chosen me in Thy mercy to watch over the life and death of Thy creatures. I now apply myself to my profession. Support me in this great task so that it may benefit mankind, for without Thy help not even the least thing will succeed."

Information for Health Professionals

Information for Patients

Modern challenged parts of the oath:

  1. To teach medicine to the sons of my teacher. In the past, medical schools gave preferential consideration to the children of physicians.
  2. To practice and prescribe to the best of my ability for the good of my patients, and to try to avoid harming them. This beneficial intention is the purpose of the physician. However, this item is still invoked in the modern discussions of euthanasia.
  3. I will not give a lethal drug to anyone if I am asked, nor will I advise such a plan. Physician organizations in most countries have strongly denounced physician participation in legal executions. However, in a small number of cases, most notably the U.S. states of Oregon,[10] Washington,[11]Montana,[12] and in the Kingdom of the Netherlands,[13] a doctor can prescribe euthanasia with the patient's consent.
  4. Similarly, I will not give a woman a pessary to cause an abortion. Since the legalization of abortion in many countries, the inclusion of the anti-abortion sentence of the Hippocratic oath has been a source of contention.
  5. To avoid violating the morals of my community. Many licensing agencies will revoke a physician's license for offending the morals of the community ("moral turpitude").
  6. I will not cut for stone, even for patients in whom the disease is manifest; I will leave this operation to be performed by practitioners, specialists in this art. The "stones" referred to are kidney stones or bladder stones, removal of which was judged too menial for physicians, and therefore was left for barbers (the forerunners of modern surgeons). Surgery was not recognized as a specialty at that time. This sentence is now interpreted as acknowledging that it is impossible for any single physician to maintain expertise in all areas. It also highlights the different historical origins of the surgeon and the physician.
  7. To keep the good of the patient as the highest priority. There may be other conflicting 'good purposes,' such as community welfare, conserving economic resources, supporting the criminal justice system, or simply making money for the physician or his employer that provide recurring challenges to physicians
http://www.worldallergy.org/educational_programs/world_allergy_forum/barcelona2008/rabe/

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