The prevalence of borderline personality disorder is estimated to range from 1. How do you know if you or someone you love suffers from one of these disorders? And how can you tell the difference? Health Matters spoke with Dr. Yeomans to define these disorders and explain the telltale signs and how to treat them.
What does borderline personality disorder look like? Those with the disorder have extremely intense emotions that can shift rapidly from a negative, depressed state to an elated one, but with a predominance of negative feeling states. The illness is also characterized by rejection-sensitivity, chaotic relationships, and an overall difficulty in managing emotions. For example, if a boyfriend or girlfriend does not return your call, instead of being annoyed and moving on, the combination of dejection and anger in a person with borderline personality disorder could possibly lead the person to cut their own wrists.
The behavioral manifestations are often self-destructive; in addition to self-cutting, substance abuse, or sexual promiscuity are common — dramatic ways of behaving that stem from not being able to manage emotions. In discussing disorders that involve changes in mood, it is important to make clear that not all depressed states indicate a psychiatric condition. In such cases, the depression may be an ongoing, terribly low, dejected mood but is appropriate to the circumstances. The borderline person demonstrates more reactivity to relatively minor events and demonstrates contradictory emotions that erupt over a short time.
How does borderline personality disorder affect relationships? People with borderline personality disorder have relationships that can be chaotic and intense, veering between a desperate neediness for others to an intense anger or dismissal of others when feeling rejected, even in situations where the other person may in fact be neutral or even positive.
There is a difficulty with how the individual perceives others. Once, when a borderline patient told me a sad story that brought tears to my eyes, he became very angry because he was convinced that my tears, rather than an expression of empathy, were my way of mocking him. Where does the behavior stem from? It comes from a combination of an emotionally charged temperament and the lack of a solid sense of self. What is the cause of this disorder? There is no single cause of borderline personality disorder, though studies suggest that certain traits, especially a temperament characterized by intense emotional reactions, stem to a large degree from genetics.
Developmental factors, including problems with emotional attunement between a developing child and caregivers, seem to play a role, as do physical or sexual abuse, or emotional neglect. Psychiatric disorders in pre-transplant phase Patients with liver failure requiring liver transplantation can have various psychological and psychiatric problems. Pre-transplant assessment Pre-transplant evaluation is used to identify psychiatric illnesses and psychological problems in the patients, 53,54 and provides an opportunity to intervene and manage them effectively.
Psychiatric evaluation Identification and management of psychiatric problems in the pre-transplant phase is very important because these have a bearing on the post-transplant outcome. Psychosocial assessment Besides core psychiatric disorders, there can be many psychosocial issues which can influence the outcome of liver transplant. Open in a separate window. Psychiatric issues as contraindications for liver transplant It is important to remember that some of the psychiatric aspects as depicted in Table 2 are considered as relative contraindications for liver transplant. Table 2 Psychiatric and psychosocial contraindications of liver transplantation.
Severe personality disorders Active substance use Active psychosis Severe neuro-cognitive disorders Suicidality Absent or inadequate psychosocial supports Demonstrated poor adherence Factitious disorder. Table 3 Role of the psychiatrist in the management of the patients of liver transplant. Appropriate treatment of the pre-existing substance use disorders and other psychiatric disorders Consideration toward possible interaction and side effects with pharmacological agents Assess for emergence of psychiatric symptoms, institute relevant management measures in case they arise Conduct psychotherapy when incorporated in management plan Enhance adherence to treatment Communicate the expectations of the treatment team to the patient and give patient's feedback to the treatment team Engage in support groups if available Develop and monitor occupational and social rehabilitation plan.
Donor related issues With time, the number of living donors for liver transplant has gradually risen. Table 4 Psycho-social evaluation of donors. Evaluation for psychiatric illnesses, past and present Assessment of psychological strengths and weaknesses Enquiry about understanding of the transplant procedure and it's implications Assessment of capacity for informed consent Relationship with the recipient and closeness Evidence of coercion or financial motivation for being a donor Availability of social supports for peri-operative period, especially if the donor is the identified caregiver for longer term.
Conclusions The numbers of liver transplantation bases has been steadily rising over time, and there is increasing emphasis on psychosocial assessment in order to improve patient outcomes. Conflicts of interest All authors have none to declare. Multidisciplinary Heidelberg Transplant Symposium. Innovations in Transplantation Medicine: Psychosocial aspects of the organ transplant experience: Effective Approaches to Patients' Behavior: Liver transplantation for alcoholic liver disease in Europe: Liver transplantation in patients with alcoholic liver disease.
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Neurological complications of liver transplantation.
II. Epidemiology of Organ Transplantation in the United States
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Psychiatric disorders before and after living-related transplantation. Psychiatric consultation for post-liver-transplantation patients. Psychological adaptation of liver transplant recipients. Association between pretransplant psychological assessments and posttransplant psychiatric disorders in living-related transplantation. Acute effects of tacrolimus FK on left ventricular mechanics.
Clinically significant drug interactions with cyclosporin. Predictive factors of alcohol relapse after orthotopic liver transplantation for alcoholic liver disease. Predictors of relapse to significant alcohol drinking after liver transplantation. Adherence in liver transplant recipients. Medication adherence in pediatric and adolescent liver transplant recipients. Impairment in cognitive function often results from end-stage organ disease and its physiologic sequelae but may also occur due to other co-morbid disease processes e.
CNS vascular disease from diabetes or hypertension , damage from prior exposures e. Prior to transplantation it is critical to attempt to differentiate between the fluctuating course of a delirium which is potentially reversible and more persistent cognitive deficits that may represent a pre-existing dementia or a static cognitive impairment. The reversibility or even progression of deficits may in part rely on age, the homeostatic reserve of the brain, prior CNS insults, and the ability to withstand future transplant related stresses e.
While the restoration of normal organ functioning and physiology post-transplant may be expected to correct the reversible cognitive impairments, deficits may take months to years to resolve [ 34 ]. In heart failure, low cardiac output and CNS hypoperfusion from reduced cerebral blood flow can contribute to cognitive impairments. Impaired cerebrovascular reactivity and ischemia may result, even in the absence of acute cerebrovascular events. Cardiac medications, including inotropic agents can also contribute to cognitive impairments. CNS microemboli are common in pre-heart transplant patients especially for those on ventricular assist devices see section on VADs.
In end-stage lung disease, hypoxia and hypercapnia may cause mild to severe cognitive deficits in these patients, particularly in the areas of executive functioning, attention and memory [ 35 ]. Oxygen therapy may improve cognitive functioning in certain candidates and these patients can benefit from lung transplantation but the extent to which these deficits are reversible is unclear [ 35 ].
Hepatic and uremic encephalopathies are two specific areas considered in detail below. Evaluation of delirium during this period of time must include careful medical examination of the patient and review of the medications and laboratory studies see Table 5. Brain imaging, EEG recording, and lumbar puncture may also provide important information.
Environmental attributes can also contribute to the development of delirium. To the extent possible, normalization of the sleep-wake cycle should be attempted in the ICU, and waking the patient during the night should be avoided unless necessary. Room lights should be off or dimmed during the night unless they are necessary to provide care to the patient. Frequent re-orientation to time and place, and reminding the patient who the staff are who are caring for the patient, and why the patient is hospitalized may also be helpful.
Whether treatment of delirium can prevent future distress or the development of delirium related PTSD symptoms is unknown. Hepatic encephalopathy HE is a specific type of delirium commonly experienced by patients with hepatic dysfunction. Symptoms of HE may be considered on a continuum from subclinical or minimal to overt and severe. Patients with hepatic encephalopathy associated with acute fulminant hepatic failure are at risk for cerebral edema, increased intracranial pressure, seizures and death pre-transplant [ 37 , 38 ]. For patients with acute liver failure who experience an acute change in mental status or progress to advanced stage hepatic encephalopathy, head computed tomography is recommended to evaluate for cerebral edema or intracranial bleed [ 40 ].
Persistent HE is rare but can be observed in patients with extensive portocaval collateral circulation or after surgical or transjugular portosystemic stent shunting procedures [ 41 ]. An electroencephalogram EEG may show common abnormalities such as generalized slowing of dominant rhythm or less commonly non-convulsive seizures; neuropsychological testing assessing psychomotor speed, praxis, concentration and attention is more efficient and perhaps more sensitive in determining minimal HE [ 38 , 40 , 42 - Weissenborn ].
HE most likely has a multifactor pathogenesis. Changes in brain metabolism and disorders of neurotransmission appear to be contributing factors. Although the predominant treatment strategy is to decrease production and absorption of ammonia in the gastrointestinal tract, it is not the only substance implicated in the pathogenesis of HE.
HE can be precipitated by significant protein intake, gastrointestinal hemorrhage causing increased protein load in the intestine , uremia, use of some psychoactive medications or diuretics, dehydration, or electrolyte imbalance [ 42 , 43 ]. Treatments should be aimed at correcting precipitating factors and should include administration of a non-absorbable disaccharide e.
Additional treatments include the use of non-absorbable antibiotics to reduce intestinal bacteria that convert protein to ammonia. A protein restricted diet may not be feasible for patients with advanced liver disease with the loss of muscle mass and cachexia. Medications which can contribute to symptoms of HE or slow intestinal motility, such as those with anticholinergic activity and opioid analgesics, should be avoided. Chronic renal failure results in multiple catabolic, metabolic, and endocrinologic processes that contribute to the development of uremic encephalopathy.
The accumulation of neurotoxic substances such as urea, uric acid, guanidine compounds, hippuric acid, indoleacetic acid and others is believed contribute to the encephalopathy; no single metabolite has been identified as the sole cause. Other pathophysiologic changes implicated in uremic encephalopathy include hormonal elevations, and electrolyte imbalances including acidosis, hyponatremia, hyperkalemia, hypocalcemia and hypermagnesemia, anemia, malnutrition, and CNS factors such as increased calcium and decreased GABA and glycine activity.
The symptoms of uremic encephalopathy typically fluctuate and can begin insidiously with patients experiencing mild cognitive impairment, irritability, or insomnia. An EEG can aid in the differential diagnosis of encephalopathy, typically showing generalized slowing of the dominant rhythm, vs. Removal of uremic toxins by hemodialysis, correction of electrolyte imbalances and anemia and the treatment of malnutrition can diminish the symptoms of encephalopathy and improve cognition.
Seizures may require treatment with anticonvulsants. Uremic encephalopathy is also associated with a cliniconeuroradiological syndrome termed posterior reversible leuko encephalopathy syndrome PRES — see section on immunosuppressive medications below. Characteristic radiographic findings on CT or MRI are seen in the posterior cortical and subcortical white matter.
Risk factors for PRES in renal patients include abrupt changes in blood pressure, autoimmune disorders, thrombotic thrombocytopenic purpura, infections specifically viral and sepsis, and nonspecific renal inflammatory conditions e. Early recognition allows corrective action to be taken. Prompt treatment may avoid potentially permanent brain damage. The extreme shortage of donated hearts and the growing list of heart transplant candidates indicates that ventricular assist device VAD therapy will play an increasingly significant role in the treatment of end-stage heart disease.
Progress in the development of VADs from external or paracorporeal devices to implantable devices has dramatically improved both the physical and psychological health of patients with end-stage heart failure.
Liver Transplant—Psychiatric and Psychosocial Aspects
While these devices are primarily used as bridges to transplantation, they can also bridge a patient to recovery e. The newest VADs now include implantable left ventricular or biventricular versions that have been miniaturized and have improved patient mobility, easy of wearability, and routinely allow discharge from the hospital. Portable pneumatic drivers and battery packs are compact and lightweight and can be worn on a shoulder strap or towed on a luggage-type carrier. Patients can also achieve significant gains in physical and physiological rehabilitation and rebuild muscle mass, potentially stabilizing their cardiac condition [ 45 ].
Many patients can engage in light to moderate physical activity including walking, driving, dancing and even work. However, despite improvements in quality of life, mobility, and functioning for VAD patients, psychological and cognitive problems are not uncommon. In the first 1—2 weeks post-implant while patients are often in the ICU they report coping well with the VAD and having low symptoms of distress but feel as if they were not doing as well as they had anticipated prior to VAD implantation [ 46 ]. Adjusting to the VAD can be psychologically difficult.
Incorporating the machinery into their body can evoke feelings of a damaged body image and sense of self and these feelings can be especially traumatic if the VAD implantation is in response to an emergency [ 47 ]. Patients can feel vulnerable, apprehensive with the machinery sounds and alarms, and can fear a VAD malfunction [ 47 ]. While patients may be too ill before implantation, psychotherapy afterwards to address these issues may ease the transition onto a VAD and help them prepare for eventual transplant.
While patients bridged to transplantation with a VAD have similar post-transplant physical recovery and emotional well-being as patients who never required VAD support, they may have poorer residual cognitive functioning post-transplant [ 48 , 49 ]. Cognitive impairments may in part be due to the higher risk of thromboembolism while supported on a VAD.
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While there is a low incidence of thromboembolic complications 0. Using cognitive P evoked potentials as a general indicator of neurocognitive functioning, one study showed in the short term VAD implantation could improve neurocognitive impairment by the time patients left the ICU [ 51 ]. Nevertheless, while many of the microembolic events are clinically silent [ 50 ] the chronic effect of microembolic events i.
Although it is not feasible to repeatedly perform computed tomography of the brain, transcranial Doppler may be beneficial for predicting the risk and periodic neuropsychologic or cognitive testing may identify silent cerebral infarctions [ 49 ]. While psychiatric symptoms may seem to be normal reactions to significant stresses of the transplant experience, lack of timely diagnosis and treatment can lead to unneeded suffering, reduced adherence to medical care, heightened physical pain, and greater functional impairment.
Nevertheless it is a complex challenge to identify and correct underlying pathophysiologic processes first that could be causing or contributing to psychiatric symptoms. If medications are needed to treat psychiatric symptoms, careful consideration must be given to the choice of medication, symptoms to be treated, the side effects of the medications, adverse drug interactions and the type and severity of organ failure with respect to alteration in pharmacokinetics.
A full discussion of this topic is beyond the scope of this chapter Table 8 provides some guidelines and suggestions. In these cases psychiatric consultation can assist in the diagnosis and selection and monitoring of psychotropics. Brief psychotherapy, even in the ICU setting may also be beneficial. In cases of delirium and other psychotic symptoms it is important to avoid medications that may worsen symptoms.
Low doses of typical and atypical antipsychotics may be most appropriate in these circumstances. Haloperidol, risperidone and quetiapine are common choices, depending upon the route of administration available [ 52 ]. Haloperidol may be given parenterally or orally. The lowest possible doses of this medication are suggested as it may cause extrapyramidal parkinsonian symptoms, akathisia and neuroleptic malignant syndrome.
Short-acting risperidone and quetiapine are currently only available in oral forms. Risperidone and olanzepine are available in a quick dissolving tablet that dissolves in seconds when placed on the tongue and may be useful if swallowing pills is a problem. These medications still need to be swallowed after dissolution and require an intact gastrointestinal tract for absorption.
Atypical antipsychotics can cause or worsen hyperglycemia and hyperlipidemia which can also be side effects of immunosuppressive medications and they also carry a small risk of QT prolongation [ 52 ]. When treating delirium regular scheduled doses of medication are preferable to as needed prn doses to stabilize symptoms.
Delaying treatment until symptoms become problematic and then using prn dosing may create a situation in which higher doses are needed to control behaviors. Large fluid volume shifts, the combined nephrotoxicity of other medications and frequent use of diuretics make use of lithium potentially dangerous and impractical. Divalproex has many drug interactions and also a small risk of hepatotoxicity.
Its use in patients with liver disease is not recommended. Side effects of divalproex include thrombocytopenia, nausea, vomiting and ataxia. Atypical antipsychotics can effectively treat symptoms of mania, psychosis, and mood dysregulation in these patients. Anxiety symptoms may be safely treated short-term with benzodiazepines; however use of these medications may cause or worsen symptoms of delirium and cognitive impairment. If a benzodiazepine is used, a short-acting medication with no active metabolites is suggested such as lorazepam.
The lowest possible dose for the shortest period of time is suggested. As with delirium, treating anxiety with a regularly scheduled medication, rather than prn, may allow more consistent alleviation of symptoms and avoid an escalation of symptoms or a requirement for a higher dose. For those patients with pre-existing alcohol or benzodiazepine addiction, care must be taken with longer-term use of benzodiazepines in order to avoid precipitating a relapse of the addiction. In general, while benzodiazepines are quick acting and effective for immediate treatment of anxiety, for patients with more persisting anxiety consideration of a non-addicting agent for longer term use is suggested.
Both anxiety and depression may be treated with selective serotonin reuptake inhibitors SSRIs e. These medications are relatively safe in the medically ill patient; however it is important to be aware that fluoxetine has a relatively long half-life and that fluoxetine, paroxetine and sertraline may have cytochrome P drug-drug interactions with medications typically administered to these patients. Venlafaxine has relatively few drug-drug interactions but in high doses may worsen hypertension. Fluvoxamine and nefazodone have very significant interactions with calcinurein inhibitors and should be avoided [ 53 ].
Bupropion may increase the risk for seizures at higher doses and can cause symptoms of restlessness or tremulousness. It should be used cautiously during the immediate peri-transplant period until the patient is stable. Calcineurin-inhibiting immunosuppressive medications CIIs are the mainstay of immunosuppressive medication regimens for most solid organ transplant recipients. Moderate to severe neuropsychiatric side effects i. The etiology of CII neurotoxicity is unclear, most likely multifactorial, and may involve biochemical or physiologic derangements or direct or indirect neurotoxic processes e.
CII neurotoxicity has been associated with biochemical and electrolyte derangements including higher plasma levels, intravenous administration, hypocholesterolemia and hypomagnesemia [ 54 ]. Disruption of the blood-brain barrier—whether structural e. Correcting the metabolic disturbance or decreasing the drug blood level can result in a resolution of symptoms, although for severe symptoms the type of CII may need to be switched e.
Anticonvulsants can successfully treat CII-induced seizures and are not required long-term. Seizures may cease if reduction or discontinuation of the drug is possible [ 54 ]. Treatment of mild symptoms can include sleep medications for sleep disruption or benzodiazepines or beta-blockers if the cardiovascular system can tolerate beta blockade for symptoms of anxiety, tremor, or restlessness. These treatments should be short-termed with the expectation that the majority of symptoms due to CII side effects will spontaneously resolve as the CII blood levels are reduced in the early post-transplant phase.
The longer term use of benzodiazepines is not recommend for symptoms of tremor, anxiety, or restlessness as the ability to satisfactorily taper the patients off of these medications at a later point, especially after they develop physiologic and psychologic dependence becomes problematic.
Symptoms of cognitive impairment, agitation, and delirium can be treated with haloperidol or atypical antipsychotics. Psychiatric consultation is recommended to assist in the correct diagnosis and choice of appropriate medication therapy see Table 8. CIIs have also been associated with a cliniconeuroradiological syndrome termed posterior reversible leuko encephalopathy syndrome PRES. Clinical symptoms can be varied ranging from mental status changes to focal neurological symptoms. Specific findings on MRI fluid attenuation inversion recovery FLAIR sequences and apparent diffusion coefficient ADC mapping sensitive to water diffusion provide further evidence towards the theory of neurotoxicity involving a vasogenic edema and may help in comparison to diffusion weighted MRI images DWI in distinguishing vasogenic from cytotoxic edema [ 55 ].
Although PRES usually occurs in the early post-operative period it can also occur years later. Both symptoms and radiologic findings can resolve with discontinuation of the CII. Finally, a rare, severe multifocal demyelinating sensorimotor polyneuropathy has been seen in patients treated with CIIs and can occur within weeks post-transplant. Polyneuropathies in general can be severely limiting, may impair physical recovery and could play a role in the liberation from mechanical ventilation. Early recognition of the symptoms is critical to recovery and sensitive electrophysiological testing may be required.
Many of these CII polyneuropathies can improve or be reversed following drug discontinuation, plasmapheresis or intravenous immunoglobulin IVIG , suggesting an immune-mediated cause e. Behavioral and psychiatric side effects of corticosteroids well described but conclusions regarding the incidence, characteristic effects, or the specific dosages required to cause such effects are not well established. The average length of time from the institution of steroid therapy to the onset of steroid psychosis is 6 days [ 60 ].
Pre-existing personality disturbances, psychiatric disorders, or prior history of steroid psychosis does not clearly increase risk [ 58 , 60 ]. Similar to the treatment of CII side effects, the treatment of steroid induced symptoms should target specific symptoms with the expectation that therapy will only be required during steroid therapy. For most transplant patients steroids can be dramatically reduced or eliminated which should alleviate the symptoms. The use of sleep medications or benzodiazepines may be effective short-term. Serotonin reuptake inhibiting antidepressants can be more safely used long-term for symptoms of depression, anxiety, or mood dysregulation but may require 3—4 weeks to become effective.
Living donors may be related to the recipient biologically e.
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Living donors constitute a unique patient population in that they are healthy individuals who receive a major surgical intervention solely for the benefit of another person. Because it is critical to minimize both the psychological and the physical risks for these individuals, they receive not only careful medical evaluations but careful psychosocial assessments in order to determine their suitability and willingness to donate. However, even the healthiest donors can have medical or psychiatric complications perioperatively or later in their recovery. Before considering psychiatric sequelae in particular, it is noteworthy that the general medical outcomes of living donor surgery show an increasingly favorable profile, especially in kidney and liver donors [ 64 , 65 , 66 , 67 ].
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The literature in other types of donors e. The perioperative mortality rate among kidney donors is 0. Minor perioperative complications e. While there are greater risks when donating a portion of the liver [ 64 , 68 ] the perioperative mortality rate for living liver donors is low - 0.
While the very long-term medical outcomes of liver donation are not yet known, the liver regenerates and thus the risk of long-term hepatic damage is believed to be low [ 67 ]. However, long-term followup data remain sparse even for kidney donors. These disturbances include delirium, anxiety, depression and—rarely—psychosis. It should be noted that these rates are generally based on referrals for psychiatric evaluation and likely underestimate the actual numbers of donors experiencing psychiatric distress early in their recovery from surgery.
Donors frequently comment that their perioperative pain was much greater than they had expected [ 75 , 76 ]. In addition, due to the perioperative steroids used to reduce inflammation, donors may experience restlessness, agitation, insomnia, and emotional lability see section on side effects of corticosteroids above. Because donors are healthy before donation, they may be more alert and less impaired post-operatively and can be more observant of the sights and sounds of the ICU environment which can be emotionally disturbing.
Thus ICU staff should be attentive to donor psychic and physical discomfort. Donors should be asked about their emotional state and level of pain, and every effort should be made to alleviate pain and psychiatric symptoms or distress. Psychiatric or pain management consultation may be sought to assist in order to assure their comfort. Despite these stresses the majority of donors return to their former high levels of well-being following the initial recovery period after donation [ 77 , 78 , 79 ], and extremely few donors report that they regret having donated.
They frequently report psychological benefits from donation, including the gratification they experience in being able to help another person, and feelings of increased self-esteem [ 80 , 81 , 82 ]. The emphasis on aggressive if not sometimes heroic treatment of complications following transplantation is understandable given the general goal of medical care to protect and sustain life.