Clinic Patient

[analgold09]

I am a medicine intern following a patient in continuity clinic who I'd like to get your thoughts on.

Pt is a 21 y/o M w/ med hx of congenital "vanishing testes" who I started seeing 4 months ago after he outgrew the peds clinic. At the time, he c/o depression, citing "not being able to live a normal life," with passing suicidal thoughts but no immediate intent or plan. I thought about SSRIs for him but instead referred him to endo for testosterone replacement, as I felt that this might be contributory to his depression.

I have seen him 2-3 times since then, and he always remained at his "depressed" baseline. Each time, he has refused psych referral ("that has never worked for me" "no one will ever understand"). My response was to schedule frequent appts with him, so he could talk even if just for 15 minutes. I'm surprised that he has kept every appt.

Today, I saw him again and felt that something was amiss. He was tearful as per normal, but our conversation was unchanged in content -- "I hate my life" "I don't even know why I keep going" -- except for the disturbing addition of: "you won't see me after the summer." I asked what he meant, and he did not elaborate. But when I probed about SI/plan (immediate and in the upcoming weeks), he unequivocally denied. His testosterone has normalized, and I started him on an SSRI, went over a safety plan and told him to come back in 2 wks.

Still, I feel so uneasy about this patient. He said all the right things, but I am paranoid that he is mollifying me and not being totally honest. I feel like I'm over my head and cannot shoulder the burden of being his defacto psychiatrist, in terms of time (his issues go beyond a 15 minute visit) and emotional toll.

Would you have done anything differently? How should I manage him best? How do I connect him with a psychiatrist when he so adamantly refuses to go?

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[Encephalopathy]

I think you're handling the case well. Is there an attending who's aware of him?

How to get him to a psychiatrist is tough. I would sell it like: you have depression with suicidal thoughts, you're on a psychotropic, you need to be treated by someone who's trained in that. Maybe he's had bad psychiatrists in the past, tell him it's just a matter of finding one that he likes.

Were his testes really vanished or do the parentheses indicate a body dysmorphic/psychotic type thing?

 

[kugel]

Just FYI for those wondering about Vanishing Testes syndrome:

(from: Kronenberg: Williams Textbook of Endocrinology, 11th ed)
Anorchia (Vanishing Testis Syndrome)
Anorchia refers to the absence of testicular tissue in a 46,XY phenotypic male. These patients have normal external male genitalia and normal wolffian duct structures and complete absence of müllerian duct structures, [133] [134] indicating that during critical periods of sexual differentiation, the testes must have present and producing testosterone and müllerian inhibiting hormone. The pathogenic factors that cause the testes to atrophy and vanish are not known. Familial occurrence and the association of anorchia with 46,XY gonadal dysgenesis have led to speculation that genetic factors associated with testis determination or descent may be involved. [135] [136] However, mutations of SRY, INSL3, and LGR8 (the receptor for INSL3) have not been found in analyses of small samples of patients with anorchia.[137] The prevalence rate of one in 20,000 men for bilateral anorchia and one in 5000 for unilateral anorchia have been reported,[134] but it is possible that the prevalence rates are higher because some cases of anorchia may be mislabeled cryptorchia.

In men with the 46,XY karyotype and nonpalpable testes, a systematic effort to locate the testes is necessary. Measurements of müllerian inhibiting substance, an hCG stimulation test with measurements of testosterone, and magnetic resonance imaging (MRI) scan of the abdomen can help locate an intra-abdominal testis. If the hCG stimulation test and MRI scans do not confirm the presence of an intra-abdominal testes, laparoscopic examination or in some instances exploratory laparotomy may be required to locate the testes and to reposition and anchor them in the scrotum.

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(From: Wein: Campbell-Walsh Urology, 9th ed.; Chapter 128 - Sexual Differentiation: Normal and Abnormal > ... > Disorders of Gonadal Differentiation and Development)

Embryonic Testicular Regression and Bilateral Vanishing Testes Syndromes
The syndromes of embryonic testicular regression and bilateral vanishing testes are characterized by patients with a 46,XY karyotype and absent testes in whom there is clear evidence of testicular function at some point during embryogenesis. The syndrome entails the presence of testes that “vanish” during embryogenesis and is distinguished from pure gonadal dysgenesis, in which there is no evidence of testicular function in utero.

These syndromes have been regarded as synonymous by some authors. Other authors, including Migeon and colleagues (1994) , have suggested a rational stratification whereby “embryonic testicular regression” refers to loss of testicular tissue within the first trimester and is associated with ambiguity of external genitalia, whereas “bilateral vanishing testes syndrome” refers to individuals in whom male sexual differentiation of ducts and genitalia took place but loss of testicular tissue occurred subsequently in utero.

The etiology of these disorders remains unclear. It is possible that regression of the testes in utero is caused by a genetic mutation, a teratogen, or bilateral torsion. A genetic cause is supported by the finding of familial instances of XY agonadism that might be consistent with the rare recessive trait. Marcantonio and associates (1994) suggested the possibility that embryonic testicular regression represents a variant of 46,XY gonadal dysgenesis. They noted a group of patients with absent testes but evidence of incongruity between the extent of Leydig cell and Sertoli cell function, suggesting that gonadal tissue in these subjects was intrinsically abnormal before the testicular regression occurred. The occurrence of embryonic testicular regression in several subjects from one family in their series suggested a genetic basis for the condition, and the pattern of inheritance implicated the involvement of an X chromosome gene. In another group of patients, these authors noted multiple congenital anomalies, suggesting either a mutation in a single gene that functions in several developmental pathways or a defect of multiple genes that might be the result of a large chromosomal deletion.

Clinically, these two syndromes represent a spectrum of phenotypes ranging in severity from complete female, to varying degrees of genital ambiguity in the embryonic testicular regression syndrome, to a normal male phenotype with microphallus and empty scrotum in the bilateral vanishing testes syndrome ( Edman et al, 1977 ). The diagnosis can be made on the basis of a 46,XY karyotype and castrate levels of testosterone despite persistently elevated serum LH and FSH ( Jarow et al, 1986 ). In the most severe form of embryonic testicular regression syndrome, agonadism is discovered in a 46,XY phenotypic female with no internal genital structures. This picture is presumed to result when the testis has elaborated MIS but vanishes at approximately day 60 to 70 of gestation, before the elaboration of androgen. In this setting, a belated Jost model is created and the individual goes on to develop a sexually infantile female phenotype but lacks any internal ductal structures. At an intermediate point in the clinical spectrum is the 46,XY patient with absent gonads and internal ductal structures but with ambiguous genitalia owing to incomplete elaboration of androgen by the vanishing testes. Finally, in bilateral vanishing testes syndrome, patients may present as agonadal XY phenotypic males with fully developed wolffian structures, but an empty scrotum, absent prostate, and microphallus. This represents testicular loss after complete anatomic development of the male external genitalia within the first trimester.

On surgical exploration of patients with bilateral vanishing testes syndrome, rudimentary cord structures are usually identified and biopsy of their distal ends demonstrates no recognizable testicular tissue histologically ( Bergada et al, 1962 ). Atrophic epididymal remnants are occasionally seen.

The management of patients with embryonic testicular regression syndrome or bilateral vanishing testes syndrome is dictated by their position in the clinical spectrum of either disorder. Sexually infantile phenotypic females require estrogen supplementation at the time of expected puberty for development of secondary sexual characteristics and may require vaginal dilation or vaginoplasty. Similarly, phenotypic males require long-term androgen replacement beginning at the time of expected puberty. A study of 21 males so treated demonstrated that replacement therapy started at the correct time caused a normal pubertal growth spurt with normal secondary sex characteristics including penile growth, together with normal bone maturation ( Aynsley-Green et al, 1976 ). In addition, these patients may benefit from placement of testicular prostheses. Patients with embryonic testicular regression syndrome and ambiguous genitalia require individualized assessment to determine the optimal gender assignment.

 

[sunlioness]

Would he see a therapist? Because honestly, I think connecting him to a competent psychotherapist with whom he "clicks" might be more helpful than anything. Also sometimes people aren't as intimidated by therapists as they are by psychiatrists for some reason. So a reasonable compromise might be that you continue his SSRI, but he sees someone for psychotherapy too.